Lung cancer is the most frequent cause of cancer-related mortality worldwide.Nitric oxide(NO),prostaglandins(PGs),thromboxanes(TXs),and endothelins(ETs)participate in numerous physiological processes.These agents play...Lung cancer is the most frequent cause of cancer-related mortality worldwide.Nitric oxide(NO),prostaglandins(PGs),thromboxanes(TXs),and endothelins(ETs)participate in numerous physiological processes.These agents play an important role in lung carcinogenesis by regulating cancer cell proliferation,apoptosis,invasion,and angiogenesis.NO is a gaseous free radical with tumo-ricidal and tumorigenic activities in lung cancer.Arachidonic acid-derived PGs,including PGD2,PGE2,8-iso-PGF2α,and PGI2,are related to the development of lung cancer.PGD2 and PGI2 act as tumor suppressors,while PGE2 and 8-iso-PGF2αpromote tumor progression.TXA2 catalyzed by cyclooxygenase induces prolif-eration as well as angiogenesis.Elevated levels of TXB2,an inactive metabolite of TXA2,are positively correlated with lung carcinoma stages.ET-1 and ET-2 are 21 amino acid polypeptides;their silencing hinders lung cancer cell proliferation and invasion.ET-2 depletion also triggers apoptotic death.This chapter review aims to provide a comprehensive overview of the role of NO,PGs,TXs,and ETs in lung cancer.展开更多
Endothelins are a family of 21‐amino acid oligopeptides,called endothelin‐1(ET‐1),endothelin‐2(ET‐2),and endothelin 3(ET‐3).Endothelins act on hepatocytes,liver endothelial cells,and Kupffer cells in a paracrine...Endothelins are a family of 21‐amino acid oligopeptides,called endothelin‐1(ET‐1),endothelin‐2(ET‐2),and endothelin 3(ET‐3).Endothelins act on hepatocytes,liver endothelial cells,and Kupffer cells in a paracrine or autocrine manner through two G protein‐coated receptors,called endothelin A and B receptors,which are mainly located in interlobular veins,interlobular artery endothelial cells and hepatic stellate cells(HSCs).ET B receptor(ETBR)‐1 is responsible for the induction of endothelial nitric oxide synthase,resulting in nitric oxide release and vasodilatation,whereas ETBR‐2 is located on HSCs and is responsible for vasoconstriction.Endothelins are not stored in the organs.Approximately 20%of endothelins are secreted into the circulation system,and are rapidly cleared by the lungs,liver,heart,and kidneys.As a potent vasoconstrictor,endothelins may have a key role for the treatment of hypertensive vascular diseases,inflammation,fibrosis,and metabolic diseases.By clearing ET‐1 from the circulation,endothelin A receptor(ETAR)antagonists can reduce intraportal vascular resistance by dilatating the portal vein,reducing the contraction of HSCs,increasing the diameter of sinusoids,facilitating the regression of liver fibrosis,and restoring liver parenchyma.ET‐1 induces nitric oxide synthase and upregulates cyclooxygenase 2 mRNA levels,making it a key factor during the onset of fibrosis and in the prognosis of patient outcomes.Endothelins can be used to treat porto‐pulmonary hypertension,portal hypertension,angiogenesis,and liver fibrosis and have been approved for the treatment of porto‐pulmonary hypertension.Endothelins are produced on mesangial cells,podocytes,tubular epithelium,and renal collecting tubes in high amounts.Activation of ETAR supports the progression of kidney diseases,whereas activation of ETBR has protective effects on the kidneys.ET‐1 plays an important role in normal cardiovascular homeostasis.Endothelins are closely associated with severe systemic hypertension,congestive heart failure,atherosclerosis,and pulmonary hypertension.Dual ET receptor antagonists reduce blood pressure,but have several side effects,including liver toxicity,acute liver failure,accumulation of salt and water,testicular toxicity,headache,and teratogenicity.Liver enzymes should be checked in all patients who have received ET receptor antagonists,and women of childbearing years should use contraception.展开更多
In the article titled“Astrocytic endothelin-1 overexpression impairs learning and memory ability in ischemic stroke via altered hippocampal neurogenesis and lipid metabolism,”published on pages 650-656,Issue 3,Volum...In the article titled“Astrocytic endothelin-1 overexpression impairs learning and memory ability in ischemic stroke via altered hippocampal neurogenesis and lipid metabolism,”published on pages 650-656,Issue 3,Volume 19 of Neural Regeneration Research(Li et al.,2024),there were two errors that needed to be corrected.展开更多
BACKGROUND Chronic pancreatitis(CP)accompanied with persistent abdominal pain represents a major clinical challenge for the symptom management in patients.Although with clear involvement of neuropathy,the detailed mec...BACKGROUND Chronic pancreatitis(CP)accompanied with persistent abdominal pain represents a major clinical challenge for the symptom management in patients.Although with clear involvement of neuropathy,the detailed mechanisms underlying pain hypersensitivity associated with CP are not totally clear.The endothelin system has been reported to contribute to chronic pain and chronic inflammatory settings,and is a potential therapeutic target for the treatment of chronic pain.AIM To evaluate the role of nociceptor-specific endothelin A receptor(ETAR)in pain hypersensitivity in a CP mouse model and its potential contributing mechanisms.METHODS Oral gavage delivery of dibutyltin dichloride(DBTC)was used to induce CP in mice.A conditional knockout(CKO)strain which specifically delete ETAR in dorsal root ganglion(DRG)nociceptive neurons was generated.Abdominal pain hypersensitivity associated with CP and other behaviors were evaluated.The size of mouse gallbladder was measured and pancreatic histopathology was examined to validate the CP model.Calcitonin gene-related peptide expression and immune cells in the innervated DRGs and spinal cord were also examined.Calcium imaging in dissociated DRG neurons was performed to investigate the excitability of affected nociceptive neurons.RESULTS Specific deletion of endothelin receptor type A gene in nociceptive DRG neurons did not affect basal abdominal thermal and mechanical pain threshold in mice.Abdominal mechanical pain hypersensitivity was persistent in DBTC-treated WT mice but was significantly reduced in DBTC-treated CKO mice.DBTC treatment did not affect mouse nociceptive responses to heat and cold stimuli,as well as motor functions and anxiety-like behaviors of mice.DBTC treatment induced severe pancreatic inflammation and obvious gallbladder enlargement in wild type(WT)mice,but less in CKO mice.DBTC-induced increase of calcitonin gene-related peptide-and induction of brown adipocytes 1-positive signals in the DRG and spinal cord in WT mice were remarkably attenuated in CKO mice.DRG neurons from CKO mice exhibited less excitability and sensitivity in response to endothelin-1 exposure than those from WT mice.CONCLUSION DBTC intragastric administration in mice produced a convenient and reliable animal model for studying abdominal pain associated with CP.ETAR-dependent endothelin signaling in nociceptors is important for the development of persistent abdominal mechanical hypersensitivity in mice.展开更多
Objective: To explore the changes of plasma endothelin(ET) and nitric oxide (NO) levels in patients with a-cute pancreatitis.Methods: The level of plasma ET was measured by ra-dioactive-immunoassay, and NO by spectrop...Objective: To explore the changes of plasma endothelin(ET) and nitric oxide (NO) levels in patients with a-cute pancreatitis.Methods: The level of plasma ET was measured by ra-dioactive-immunoassay, and NO by spectrophotometry.Results: The levels of ET, NO and the ET/NO ratioin patients with severe acute pancreatitis(SAP) within24 hours in hospital were all significantly higher thanthose in other groups of patients [(176±8)pg/ml,(97±11) μmol/L, and 1.83±0.12, P<0.01]. Com-pared to healthy controls(N), the levels of ET and NOin patients without pancreatitis acute abdomen (NAP)and patients with mild acute pancreatitis (MAP) in-creased significantly (P<0.01). After appropriate treat-ment, the levels of ET and NO in the MAP groupwere lower (P<0.01). Compared with those beforetreatment, the levels of ET and NO in the SAP groupon the 3rd and 7th day in hospital dropped signifi-cantly(P<0.01).The ET/NO ratio on the 7th daywas also lower than that on admission (P<0.01).Conclusions: The malfunction of endothelial cells andthe increased ET/NO ratio may be related to the mecha-nism of pancreatic microcirculatory disturbance in pa-tients with SAP; early dynamic determination of theseparameters may help predict the prognosis of SAP.展开更多
INTRODUCTIONPortal hypertension is a common clinical syndromecharacterized by an abnormal increase in portalblood to the systemic circulation, bypassing theliver. Recent studies have reported that humoralsubstances pl...INTRODUCTIONPortal hypertension is a common clinical syndromecharacterized by an abnormal increase in portalblood to the systemic circulation, bypassing theliver. Recent studies have reported that humoralsubstances play an important role in thepathogenesis of portal hypertension, either byincreasing vascular resistance at both theintrahepatic and porto-collateral sites or affectingsplanchnic vasodilation with a concomitant increasein parto-collateral blood flow[1-6]展开更多
In the cerebral hemorrhage model rats established by injection of collagenase and heparin into caudate nucleus, the effects of electroacupuncture (EA) on the contents of nitric oxide (NO) and endothelin (ET),and total...In the cerebral hemorrhage model rats established by injection of collagenase and heparin into caudate nucleus, the effects of electroacupuncture (EA) on the contents of nitric oxide (NO) and endothelin (ET),and total anti-oxidation capability (T-AOC) in the brain tissues were investigated. It is found that the content of NO in the Shuigou EA group lowered, ET decreased and the T-AOC raised significantly in both the Fengfu EA group and the Shuigou EA group (all P＜0.05) as compared with the model group,indicating that acupuncture can reduce the contents of ET and NO, and increase the T-AOC in the brain tissues of the rats with cerebral hemorrhage.展开更多
目的观察化痰祛浊通络方对自发性高血压大鼠(SHR)血压及一氧化氮(NO)、内皮素1(ET-1)及血管紧张素Ⅱ(AngⅡ)的影响,探讨其降压作用机制。方法将15月龄SHR随机分为空白对照组、化痰祛浊通络方组和吲达帕胺组,每组各9只。空白对照组予0.9...目的观察化痰祛浊通络方对自发性高血压大鼠(SHR)血压及一氧化氮(NO)、内皮素1(ET-1)及血管紧张素Ⅱ(AngⅡ)的影响,探讨其降压作用机制。方法将15月龄SHR随机分为空白对照组、化痰祛浊通络方组和吲达帕胺组,每组各9只。空白对照组予0.9%氯化钠注射液(10 m L/kg)、化痰祛浊通络方组予化痰祛浊通络方水煎液(生药10 m L/kg)、吲达帕胺组予吲达帕胺溶液(10 mg/kg),均每日1次灌服,连续6周。所有大鼠每周测量尾动脉压,给药6周腹主动脉抽血测定血清NO、ET-1及AngⅡ含量。结果给药6周后,化痰祛浊通络方组和吲达帕胺组给药后均可降低SHR收缩压(SP)和舒张压(DP),与空白对照组及本组给药前比较差异均有统计学意义(P<0.05);化痰祛浊通络方组及吲达帕胺组ET-1和AngⅡ含量均较本组给药前及空白对照组明显降低,NO含量明显升高,差异均有统计学意义(P<0.05)。结论化痰祛浊通络方能明显降低SHR血压,其机制可能是通过下调ET、AngⅡ含量及上调NO含量来发挥降压作用。展开更多
In order to inquire into the therapeutic effects of Xin Mai Tong Capsule (心脉通胶囊) on coronary heart disease with myocardial ischemia, 40 patients were randomly divided into two groups (Xin Mai Tong group and the c...In order to inquire into the therapeutic effects of Xin Mai Tong Capsule (心脉通胶囊) on coronary heart disease with myocardial ischemia, 40 patients were randomly divided into two groups (Xin Mai Tong group and the control group). The plasma endothelin (ET) levels in the two groups of patients were markedly higher than that of the healthy people (P<0.001), and the calcitonin gene related peptide (CGRP) was similar to that of the healthy people (P>0.05). After treatment, ET and symptomatic scores in the two groups decreased markedly (P<0.01), and their S-T segments were elevated obviously (P<0.01). But the decrease of ET and symptomatic scores and elevation of S-T segment in Xin Mai Tong group were superior to those of the control group (P<0.05～0.01). The CGRP level in the control group did not vary obviously post-treatment, but it increased markedly (P<0.01) with the addition of Xin Mai Tong Capsule in Xin Mai Tong group.展开更多
To investigate the therapeutic effects and mechanisms of garlicin for treatment of unstable angina pectoris (UAP), garlicin injectio was intravenously dripped 60 mg/day in 34 cases for 10 days. Nitroglycerine was used...To investigate the therapeutic effects and mechanisms of garlicin for treatment of unstable angina pectoris (UAP), garlicin injectio was intravenously dripped 60 mg/day in 34 cases for 10 days. Nitroglycerine was used in 21 cases of the control group. The results showed that the total effective rates in improving symptoms and electrocardiogram after garlicin treatment were respectively 82% and 62%, and that the plasma endothelin and blood sugar levels were markedly lowered in cases with hyperglycemia.展开更多
AIM: To investigate the relationship between primary afferent neurons, endothelin (ET) and the role of its receptors on ethanol-induced gastric damage in cirrhotic rats. METHODS: Cirrhosis and portal hypertension were...AIM: To investigate the relationship between primary afferent neurons, endothelin (ET) and the role of its receptors on ethanol-induced gastric damage in cirrhotic rats. METHODS: Cirrhosis and portal hypertension were induced in rats by bile duct ligation (BDL) while controls had a sham operation. The association between ET and afferent neurons on the gastric mucosa was evaluated by capsaicin treatment in newborn rats, the use of ET agonists or antagonists, gastric ET-1 and -3 mRNA and synthetic capacity. Ethanol-induced damage was assessed using ex vivo gastric chamber experiments.Gastric blood flow was measured by laser-Doppler flow-metry. RESULTS: ET-3 and an ETB receptor antagonist sig- nificantly reduced the extent of ethanol-induced gastric damage in BDL rats. Gastric ET-1 and -3 levels were 30% higher in BDL rats compared to control rats. Cap-saicin treatment restored the gastric resistance and blood flow responses to topical application of ethanol in BDL rats and ET-1 and -3 production to levels observed in controls. CONCLUSION: Our results suggest that the reduced resistance of the gastric mucosa of cirrhotic rats to ethanol-induced injury is a phenomenon modulated by ET through the ET B receptor and by sensory afferent neurons.展开更多
Objective To probe into the impacts on the therapeutic effects and endothelin （ET） in multi-infarct dementia （MID） treated with cluster pricking on head points.Methods 60 cases of MID were randomized into acupunct...Objective To probe into the impacts on the therapeutic effects and endothelin （ET） in multi-infarct dementia （MID） treated with cluster pricking on head points.Methods 60 cases of MID were randomized into acupuncture group and western medicine group,treated with cluster pricking on head points and huperzien A tablet respectively.Plasma ET lever,HDS,ADL and CNFDS （clinical neurological functional defect scoring） were determined before treatment,and the statistical analysis showed that there were no significant difference （P〉0.05）.Results In 8-week treatment,ET level in both groups were decreased,but it was decreased much more obviously in acupuncture group,indicating significant difference in the statistical comparison （P〈0.05）.The scores of HDS and ADL were all up in acupuncture and western medicine groups,but the significant statistical difference was obtained in the comparison between acupuncture group and western medicine group （P〈0.05）.In acupuncture group,the result of CNFDS was much down comparing with that before the treatment,indicating significant difference （P〈0.05）;but in western medicine group,there was no significant difference in CNFDS before and after treatment （P〉0.05）,suggesting that acupuncture reduces CNFDS of MID patient,neither for western medicine.Conclusion Cluster pricking on head points improves the intelligence of MID patient,reduces ET level and grades up HDS and ADL,moreover,it reduces CNFDS of MID patients and releases the symptoms.展开更多
31 cases of atherosclerosis (AS) were treated with Jiang Zhi Tong Mai Fang ([symbol: see text], formula of JZTMF), and its effect was compared with 30 cases treated with lovastatin in the control group. Clinically, th...31 cases of atherosclerosis (AS) were treated with Jiang Zhi Tong Mai Fang ([symbol: see text], formula of JZTMF), and its effect was compared with 30 cases treated with lovastatin in the control group. Clinically, the JZTMF formula showed an effect of regulating blood lipids, and therefore it was antiatherosclerotic. The mechanism is, probably, restoration of the function of endothelial cells (EC) by increasing the synthesis of 6-keto-PGF1 alpha and decreasing the release of endothelin (ET) as evidenced in the experimental study.展开更多
Objective: To study the effects of heparin-coated stent (Wiktor-I) on recovering the balance between endothelin- 1(ET- 1) and calcitonin gene-related peptide (CGRP) both in the plasma of coronary sinus and peripheral ...Objective: To study the effects of heparin-coated stent (Wiktor-I) on recovering the balance between endothelin- 1(ET- 1) and calcitonin gene-related peptide (CGRP) both in the plasma of coronary sinus and peripheral vein after stent implantation. Methods: The patients with coronary artery disease (n=30) were divided into non-coated stent (NCS) group (n=16) and heparin-coated stent (HCS) group (n=14). Circulating ET-1 and CGRP levels were measured by radioimmunoassay (RIA) in the 2 groups at the paired sampling sites, namely the coronary sinus (Cs) and peripheral vein (Pv). The ratio of ET/CGRP was also calculated to reflect the balance of ET and CORP. Results: In NCS group plasma ET-1 concentrations exhibited 2 peaks at 0 mm and 12 h after stent implantation, CORP levels were highly consistent with that of ET-1, and the ratio of ET/CGRP increased markedly at post-PTCA 5 mm, persisting until post-stent 12 h. While in HCS group ET-1 levels and the ratio of ET/CGRP were decreased dramatically compared with that of NCS group at 5 min,10 mm and 12 h post-stent (P＜0.05, P＜0.01 and P＜0.05, respectively＝. There was no remarkable difference of CGRP levels between the 2 groups. Conclusions: Heparin-coated stent can decrease the post-stent circulating ET-1 levels and recover the balance between ET-1 and CGRP.展开更多
Brain microvascular endothelial cells form the interface between nervous tissue and circulating blood, and regulate central nervous system homeostasis. Brain microvascular endothelial cells differ from peripheral endo...Brain microvascular endothelial cells form the interface between nervous tissue and circulating blood, and regulate central nervous system homeostasis. Brain microvascular endothelial cells differ from peripheral endothelial cells with regards expression of specific ion transporters and receptors, and contain fewer fenestrations and pinocytotic vesicles. Brain microvascular endothelial cells also synthesize several factors that influence blood vessel function. This review describes the morphological characteristics and functions of brain microvascular endothelial cells, and summarizes current knowledge regarding changes in brain microvascular endothelial cells during stroke progression and therapies. Future studies should focus on identifying mechanisms underlying such changes and developing possible neuroprotective therapeutic interventions.展开更多
文摘Lung cancer is the most frequent cause of cancer-related mortality worldwide.Nitric oxide(NO),prostaglandins(PGs),thromboxanes(TXs),and endothelins(ETs)participate in numerous physiological processes.These agents play an important role in lung carcinogenesis by regulating cancer cell proliferation,apoptosis,invasion,and angiogenesis.NO is a gaseous free radical with tumo-ricidal and tumorigenic activities in lung cancer.Arachidonic acid-derived PGs,including PGD2,PGE2,8-iso-PGF2α,and PGI2,are related to the development of lung cancer.PGD2 and PGI2 act as tumor suppressors,while PGE2 and 8-iso-PGF2αpromote tumor progression.TXA2 catalyzed by cyclooxygenase induces prolif-eration as well as angiogenesis.Elevated levels of TXB2,an inactive metabolite of TXA2,are positively correlated with lung carcinoma stages.ET-1 and ET-2 are 21 amino acid polypeptides;their silencing hinders lung cancer cell proliferation and invasion.ET-2 depletion also triggers apoptotic death.This chapter review aims to provide a comprehensive overview of the role of NO,PGs,TXs,and ETs in lung cancer.
文摘Endothelins are a family of 21‐amino acid oligopeptides,called endothelin‐1(ET‐1),endothelin‐2(ET‐2),and endothelin 3(ET‐3).Endothelins act on hepatocytes,liver endothelial cells,and Kupffer cells in a paracrine or autocrine manner through two G protein‐coated receptors,called endothelin A and B receptors,which are mainly located in interlobular veins,interlobular artery endothelial cells and hepatic stellate cells(HSCs).ET B receptor(ETBR)‐1 is responsible for the induction of endothelial nitric oxide synthase,resulting in nitric oxide release and vasodilatation,whereas ETBR‐2 is located on HSCs and is responsible for vasoconstriction.Endothelins are not stored in the organs.Approximately 20%of endothelins are secreted into the circulation system,and are rapidly cleared by the lungs,liver,heart,and kidneys.As a potent vasoconstrictor,endothelins may have a key role for the treatment of hypertensive vascular diseases,inflammation,fibrosis,and metabolic diseases.By clearing ET‐1 from the circulation,endothelin A receptor(ETAR)antagonists can reduce intraportal vascular resistance by dilatating the portal vein,reducing the contraction of HSCs,increasing the diameter of sinusoids,facilitating the regression of liver fibrosis,and restoring liver parenchyma.ET‐1 induces nitric oxide synthase and upregulates cyclooxygenase 2 mRNA levels,making it a key factor during the onset of fibrosis and in the prognosis of patient outcomes.Endothelins can be used to treat porto‐pulmonary hypertension,portal hypertension,angiogenesis,and liver fibrosis and have been approved for the treatment of porto‐pulmonary hypertension.Endothelins are produced on mesangial cells,podocytes,tubular epithelium,and renal collecting tubes in high amounts.Activation of ETAR supports the progression of kidney diseases,whereas activation of ETBR has protective effects on the kidneys.ET‐1 plays an important role in normal cardiovascular homeostasis.Endothelins are closely associated with severe systemic hypertension,congestive heart failure,atherosclerosis,and pulmonary hypertension.Dual ET receptor antagonists reduce blood pressure,but have several side effects,including liver toxicity,acute liver failure,accumulation of salt and water,testicular toxicity,headache,and teratogenicity.Liver enzymes should be checked in all patients who have received ET receptor antagonists,and women of childbearing years should use contraception.
文摘In the article titled“Astrocytic endothelin-1 overexpression impairs learning and memory ability in ischemic stroke via altered hippocampal neurogenesis and lipid metabolism,”published on pages 650-656,Issue 3,Volume 19 of Neural Regeneration Research(Li et al.,2024),there were two errors that needed to be corrected.
基金Supported by Hansoh Foundation of Lianyungang,No.QN1913.
文摘BACKGROUND Chronic pancreatitis(CP)accompanied with persistent abdominal pain represents a major clinical challenge for the symptom management in patients.Although with clear involvement of neuropathy,the detailed mechanisms underlying pain hypersensitivity associated with CP are not totally clear.The endothelin system has been reported to contribute to chronic pain and chronic inflammatory settings,and is a potential therapeutic target for the treatment of chronic pain.AIM To evaluate the role of nociceptor-specific endothelin A receptor(ETAR)in pain hypersensitivity in a CP mouse model and its potential contributing mechanisms.METHODS Oral gavage delivery of dibutyltin dichloride(DBTC)was used to induce CP in mice.A conditional knockout(CKO)strain which specifically delete ETAR in dorsal root ganglion(DRG)nociceptive neurons was generated.Abdominal pain hypersensitivity associated with CP and other behaviors were evaluated.The size of mouse gallbladder was measured and pancreatic histopathology was examined to validate the CP model.Calcitonin gene-related peptide expression and immune cells in the innervated DRGs and spinal cord were also examined.Calcium imaging in dissociated DRG neurons was performed to investigate the excitability of affected nociceptive neurons.RESULTS Specific deletion of endothelin receptor type A gene in nociceptive DRG neurons did not affect basal abdominal thermal and mechanical pain threshold in mice.Abdominal mechanical pain hypersensitivity was persistent in DBTC-treated WT mice but was significantly reduced in DBTC-treated CKO mice.DBTC treatment did not affect mouse nociceptive responses to heat and cold stimuli,as well as motor functions and anxiety-like behaviors of mice.DBTC treatment induced severe pancreatic inflammation and obvious gallbladder enlargement in wild type(WT)mice,but less in CKO mice.DBTC-induced increase of calcitonin gene-related peptide-and induction of brown adipocytes 1-positive signals in the DRG and spinal cord in WT mice were remarkably attenuated in CKO mice.DRG neurons from CKO mice exhibited less excitability and sensitivity in response to endothelin-1 exposure than those from WT mice.CONCLUSION DBTC intragastric administration in mice produced a convenient and reliable animal model for studying abdominal pain associated with CP.ETAR-dependent endothelin signaling in nociceptors is important for the development of persistent abdominal mechanical hypersensitivity in mice.
文摘Objective: To explore the changes of plasma endothelin(ET) and nitric oxide (NO) levels in patients with a-cute pancreatitis.Methods: The level of plasma ET was measured by ra-dioactive-immunoassay, and NO by spectrophotometry.Results: The levels of ET, NO and the ET/NO ratioin patients with severe acute pancreatitis(SAP) within24 hours in hospital were all significantly higher thanthose in other groups of patients [(176±8)pg/ml,(97±11) μmol/L, and 1.83±0.12, P<0.01]. Com-pared to healthy controls(N), the levels of ET and NOin patients without pancreatitis acute abdomen (NAP)and patients with mild acute pancreatitis (MAP) in-creased significantly (P<0.01). After appropriate treat-ment, the levels of ET and NO in the MAP groupwere lower (P<0.01). Compared with those beforetreatment, the levels of ET and NO in the SAP groupon the 3rd and 7th day in hospital dropped signifi-cantly(P<0.01).The ET/NO ratio on the 7th daywas also lower than that on admission (P<0.01).Conclusions: The malfunction of endothelial cells andthe increased ET/NO ratio may be related to the mecha-nism of pancreatic microcirculatory disturbance in pa-tients with SAP; early dynamic determination of theseparameters may help predict the prognosis of SAP.
基金Project supported by the National Natural Science FoundationMinistry of Public Health of China, No. 37600481
文摘INTRODUCTIONPortal hypertension is a common clinical syndromecharacterized by an abnormal increase in portalblood to the systemic circulation, bypassing theliver. Recent studies have reported that humoralsubstances play an important role in thepathogenesis of portal hypertension, either byincreasing vascular resistance at both theintrahepatic and porto-collateral sites or affectingsplanchnic vasodilation with a concomitant increasein parto-collateral blood flow[1-6]
文摘In the cerebral hemorrhage model rats established by injection of collagenase and heparin into caudate nucleus, the effects of electroacupuncture (EA) on the contents of nitric oxide (NO) and endothelin (ET),and total anti-oxidation capability (T-AOC) in the brain tissues were investigated. It is found that the content of NO in the Shuigou EA group lowered, ET decreased and the T-AOC raised significantly in both the Fengfu EA group and the Shuigou EA group (all P＜0.05) as compared with the model group,indicating that acupuncture can reduce the contents of ET and NO, and increase the T-AOC in the brain tissues of the rats with cerebral hemorrhage.
文摘目的观察化痰祛浊通络方对自发性高血压大鼠(SHR)血压及一氧化氮(NO)、内皮素1(ET-1)及血管紧张素Ⅱ(AngⅡ)的影响,探讨其降压作用机制。方法将15月龄SHR随机分为空白对照组、化痰祛浊通络方组和吲达帕胺组,每组各9只。空白对照组予0.9%氯化钠注射液(10 m L/kg)、化痰祛浊通络方组予化痰祛浊通络方水煎液(生药10 m L/kg)、吲达帕胺组予吲达帕胺溶液(10 mg/kg),均每日1次灌服,连续6周。所有大鼠每周测量尾动脉压,给药6周腹主动脉抽血测定血清NO、ET-1及AngⅡ含量。结果给药6周后,化痰祛浊通络方组和吲达帕胺组给药后均可降低SHR收缩压(SP)和舒张压(DP),与空白对照组及本组给药前比较差异均有统计学意义(P<0.05);化痰祛浊通络方组及吲达帕胺组ET-1和AngⅡ含量均较本组给药前及空白对照组明显降低,NO含量明显升高,差异均有统计学意义(P<0.05)。结论化痰祛浊通络方能明显降低SHR血压,其机制可能是通过下调ET、AngⅡ含量及上调NO含量来发挥降压作用。
文摘In order to inquire into the therapeutic effects of Xin Mai Tong Capsule (心脉通胶囊) on coronary heart disease with myocardial ischemia, 40 patients were randomly divided into two groups (Xin Mai Tong group and the control group). The plasma endothelin (ET) levels in the two groups of patients were markedly higher than that of the healthy people (P<0.001), and the calcitonin gene related peptide (CGRP) was similar to that of the healthy people (P>0.05). After treatment, ET and symptomatic scores in the two groups decreased markedly (P<0.01), and their S-T segments were elevated obviously (P<0.01). But the decrease of ET and symptomatic scores and elevation of S-T segment in Xin Mai Tong group were superior to those of the control group (P<0.05～0.01). The CGRP level in the control group did not vary obviously post-treatment, but it increased markedly (P<0.01) with the addition of Xin Mai Tong Capsule in Xin Mai Tong group.
文摘To investigate the therapeutic effects and mechanisms of garlicin for treatment of unstable angina pectoris (UAP), garlicin injectio was intravenously dripped 60 mg/day in 34 cases for 10 days. Nitroglycerine was used in 21 cases of the control group. The results showed that the total effective rates in improving symptoms and electrocardiogram after garlicin treatment were respectively 82% and 62%, and that the plasma endothelin and blood sugar levels were markedly lowered in cases with hyperglycemia.
基金Supported by A fellowship from Fundaao de Amparo a Pes-quisa do Estado de Sao Paulo, FAPESP, Brazil (to Cmara PRS)a research grant from FAPESP (to Ferraz JGP)
文摘AIM: To investigate the relationship between primary afferent neurons, endothelin (ET) and the role of its receptors on ethanol-induced gastric damage in cirrhotic rats. METHODS: Cirrhosis and portal hypertension were induced in rats by bile duct ligation (BDL) while controls had a sham operation. The association between ET and afferent neurons on the gastric mucosa was evaluated by capsaicin treatment in newborn rats, the use of ET agonists or antagonists, gastric ET-1 and -3 mRNA and synthetic capacity. Ethanol-induced damage was assessed using ex vivo gastric chamber experiments.Gastric blood flow was measured by laser-Doppler flow-metry. RESULTS: ET-3 and an ETB receptor antagonist sig- nificantly reduced the extent of ethanol-induced gastric damage in BDL rats. Gastric ET-1 and -3 levels were 30% higher in BDL rats compared to control rats. Cap-saicin treatment restored the gastric resistance and blood flow responses to topical application of ethanol in BDL rats and ET-1 and -3 production to levels observed in controls. CONCLUSION: Our results suggest that the reduced resistance of the gastric mucosa of cirrhotic rats to ethanol-induced injury is a phenomenon modulated by ET through the ET B receptor and by sensory afferent neurons.
文摘Objective To probe into the impacts on the therapeutic effects and endothelin （ET） in multi-infarct dementia （MID） treated with cluster pricking on head points.Methods 60 cases of MID were randomized into acupuncture group and western medicine group,treated with cluster pricking on head points and huperzien A tablet respectively.Plasma ET lever,HDS,ADL and CNFDS （clinical neurological functional defect scoring） were determined before treatment,and the statistical analysis showed that there were no significant difference （P〉0.05）.Results In 8-week treatment,ET level in both groups were decreased,but it was decreased much more obviously in acupuncture group,indicating significant difference in the statistical comparison （P〈0.05）.The scores of HDS and ADL were all up in acupuncture and western medicine groups,but the significant statistical difference was obtained in the comparison between acupuncture group and western medicine group （P〈0.05）.In acupuncture group,the result of CNFDS was much down comparing with that before the treatment,indicating significant difference （P〈0.05）;but in western medicine group,there was no significant difference in CNFDS before and after treatment （P〉0.05）,suggesting that acupuncture reduces CNFDS of MID patient,neither for western medicine.Conclusion Cluster pricking on head points improves the intelligence of MID patient,reduces ET level and grades up HDS and ADL,moreover,it reduces CNFDS of MID patients and releases the symptoms.
文摘31 cases of atherosclerosis (AS) were treated with Jiang Zhi Tong Mai Fang ([symbol: see text], formula of JZTMF), and its effect was compared with 30 cases treated with lovastatin in the control group. Clinically, the JZTMF formula showed an effect of regulating blood lipids, and therefore it was antiatherosclerotic. The mechanism is, probably, restoration of the function of endothelial cells (EC) by increasing the synthesis of 6-keto-PGF1 alpha and decreasing the release of endothelin (ET) as evidenced in the experimental study.
文摘Objective: To study the effects of heparin-coated stent (Wiktor-I) on recovering the balance between endothelin- 1(ET- 1) and calcitonin gene-related peptide (CGRP) both in the plasma of coronary sinus and peripheral vein after stent implantation. Methods: The patients with coronary artery disease (n=30) were divided into non-coated stent (NCS) group (n=16) and heparin-coated stent (HCS) group (n=14). Circulating ET-1 and CGRP levels were measured by radioimmunoassay (RIA) in the 2 groups at the paired sampling sites, namely the coronary sinus (Cs) and peripheral vein (Pv). The ratio of ET/CGRP was also calculated to reflect the balance of ET and CORP. Results: In NCS group plasma ET-1 concentrations exhibited 2 peaks at 0 mm and 12 h after stent implantation, CORP levels were highly consistent with that of ET-1, and the ratio of ET/CGRP increased markedly at post-PTCA 5 mm, persisting until post-stent 12 h. While in HCS group ET-1 levels and the ratio of ET/CGRP were decreased dramatically compared with that of NCS group at 5 min,10 mm and 12 h post-stent (P＜0.05, P＜0.01 and P＜0.05, respectively＝. There was no remarkable difference of CGRP levels between the 2 groups. Conclusions: Heparin-coated stent can decrease the post-stent circulating ET-1 levels and recover the balance between ET-1 and CGRP.
基金supported by grants from the National Natural Science Foundation of ChinaNo.8117111281371272 to MCL
文摘Brain microvascular endothelial cells form the interface between nervous tissue and circulating blood, and regulate central nervous system homeostasis. Brain microvascular endothelial cells differ from peripheral endothelial cells with regards expression of specific ion transporters and receptors, and contain fewer fenestrations and pinocytotic vesicles. Brain microvascular endothelial cells also synthesize several factors that influence blood vessel function. This review describes the morphological characteristics and functions of brain microvascular endothelial cells, and summarizes current knowledge regarding changes in brain microvascular endothelial cells during stroke progression and therapies. Future studies should focus on identifying mechanisms underlying such changes and developing possible neuroprotective therapeutic interventions.
