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
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 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
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 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.
