OBJECTIVE: To observe the effect of electroacupuncture(EA) treatment on the expression of E-prostanoid 2(EP2) in the spinal cord using a rat model of neuropathic pain, and to examine the effect of different acupunctur...OBJECTIVE: To observe the effect of electroacupuncture(EA) treatment on the expression of E-prostanoid 2(EP2) in the spinal cord using a rat model of neuropathic pain, and to examine the effect of different acupuncture prescriptions.METHODS: Rats were randomly divided into six groups: a normal group, model group, sham group,EA 1 group(distal-proximal acupoints), EA 2 group(proximal acupoints), and EA 3 group(distal acupoints). Rats in the EA groups were treated for20 min, once daily for 7 days. The mechanical withdrawal threshold was evaluated at 1 day preoperatively and at 3, 5, and 7 days postoperatively. At 7days postoperatively, hematoxylin-eosin(HE) staining was used to investigate spinal morphological changes. Spinal EP2 messenger ribonucleic acid(m RNA) was detected using reverse-transcription polymerase chain reaction.RESULTS: After the EA treatment, the mechanical withdrawal threshold was up-regulated compared with the model group(P < 0.05). The expression of EP2 m RNA was up-regulated in the spinal cord on day 7 after surgery(P < 0.05). EA stimulation tended to down-regulate EP2 m RNA expression compared with the model group(P > 0.05). The EA 1and EA 2 groups showed a larger treatment effect than the EA 3 group. The HE results showed that EA can improve spinal histomorphology induced by neuropathic pain.CONCLUSION: EA had a strong analgesic and anti-inflammatory effect. The therapeutic effect of EA on the down-regulation of spinal EP2 m RNA expression may be greater when either local acupoints or a distal-proximal combination of acupoints are used than when distal points are used.展开更多
A new method for introduction to-side chain of prostanoid was described in this note. Starting from acid chloride （3）, via Barton radical reaction, a trans α,β-unsaturated ketone sython was introduced.
Many agents are known to cause qualitative and quantitative differences in intrarenal blood flow. This study tested the hypothesis that angiotensin II (AII) evokes a differential effect on cortical (CBF) and medullary...Many agents are known to cause qualitative and quantitative differences in intrarenal blood flow. This study tested the hypothesis that angiotensin II (AII) evokes a differential effect on cortical (CBF) and medullary blood flow (MBF) and that AT2 receptor mediates AII-induced increase in renal MBF by mechanisms related to nitric oxide (NO) and prostanoids. AII (100, 300 and 1000 ng/kg/min) increased mean arterial blood pressure (MABP) by 24% ± 7% (p G nitro-L-arginine (L-NNA), an inhibitor of NO synthase (100 mg/L in drinking water) enhanced AII effects on MABP (169 ± 75, p ATP channel blocker, did not affect intra-renal hemodynamics elicited by AII. Blockade of AT2 receptors with PD123319 (50 μg/kg/min) did not change basal or AII-induced changes MABP or CBF but blunted AII-induced increase in MBF by 60% ± 11 % (p 2 receptor agonist, elicited a reduction in MABP and increases in CBF and MBF that were abolished or attenuated by PD123319. These findings demonstrate that AII elicited differential changes in intrarenal blood flow;an AT1-mediated reduction in CBF but an AT2-mediated increase in MBF. The AT2 receptor-mediated increase in MBF involves guanylase cyclase, NO and dilator prostanoids but not KATP channels.展开更多
A stereoselective and regiospecific synthesis of procursors(2),(4),(6)and(7)of prostacyclin analogues from 2,3-epoxylbicyclo[3.2.0]hept-6-one(1)are described.
Background Cyclooxygenase （COX） is the rate-limiting enzyme in the production of prostanoids from arachidonic acid. COX-2 is the inducible enzyme in the COX family, together with the prostanoids forms the COX-2/pros...Background Cyclooxygenase （COX） is the rate-limiting enzyme in the production of prostanoids from arachidonic acid. COX-2 is the inducible enzyme in the COX family, together with the prostanoids forms the COX-2/prostanoid pathway. Research showed that the COX-2/prostanoid pathway is activated in hepatic diseases and liver stress reaction, such as fibrogenesis, portal hypertension, carcinogenesis, and ischemic/repeffusion injury. But there was no report on visceral pain induced liver stress. This study was to investigate the role of the COX-2/prostanoid pathway in liver stress response in rat acute colitis visceral pain liver stress model.Methods Fifty-three male SD rats were randomly divided into Naive, Model, NS398 treatment, and Morphine treatment groups. The rat acute colitis visceral pain liver stress model was established under anesthesia by the colonic administration of 0.5 ml of 6% acetic acid using a urethral catheter. NS398 and morphine were administrated 30 minutes prior to model establishment in NS398 and Morphine treatment groups respectively. Spontaneous activities and pain behavior were counted and the extent of colonic inflammation was assessed histologically. Liver tissue levels of Glutathione-S-Transferase （GST） activity, COX-2 mRNA, prostaglandin E2 （PGE2）, thromboxane B2 （TXB2） and 6-Ketone-prostaglandin F1α （6-K-PGF1α） contents were assessed.Results Thirty minutes after the colonic administration of acetic acid, a significant decrease in spontaneous activities and an increase in pain behaviors were observed in Model group （P〈0.01 and P〈0.05 respectively）, accompanied by colonic inflammation. Liver GST activity levels significantly dropped （P〈0.05）. Liver COX-2 mRNA expressi.on significantly increased, accompanied by an increase in liver concentrations of PGE2 and TXB2, but no obvious change in 6-K-PGF1α concentrations. NS398 and morphine both ameliorated post-stress liver GST activity （P〈0.05 and P〈0.01 respectively）, decreased stress-induced COX-2 expression, decreased PGE2 and TXB2 production, but increased liver 6-K-PGF1α levels. Morphine attenuation in colonic tissue inflammation was apparent at 24 hours （P〈0.05）.Conclusions Acute colitis visceral pain liver stress can induce liver injury. Liver injury might have occurred through the activation of the COX-2/prostanoid pathway and increased production of PGE2 and TXB2. Effective analgesia might offer protective effect during visceral pain stress.展开更多
Atherosclerosis is the most prevalent disease in middle and later years of human life. Heart attacks and strokes are among the most frequent causes of death. New approaches in therapy are the use of NSAID’s (nonstero...Atherosclerosis is the most prevalent disease in middle and later years of human life. Heart attacks and strokes are among the most frequent causes of death. New approaches in therapy are the use of NSAID’s (nonsteroidal antiphlogistical drugs) of the new generation (selective inhibitors of COX-2) and DHEA (Dehydroepiandrostenon). The key enzyme of prostaglandin synthesis, the COX-2 isoenzyme, is predominantly found in inflammatory tissue. Out of this results a possible importance of COX-2-inhibitors in prophylaxis of atherosclerosis. Our study intended to examine the significance of COX-2 and the COX-2-formed prostanoids, as well as the significance of COX-2-independent iso-prostanes on atherosclerosis. For that purpose we tested the effect of the selective COX-2-inhibitor Celecoxib on rabbits fed with cholesterol and compared this with the effect of the steroid hormone DHEA in 4 groups: healthy control, cholesterol-fed control, DHEA-group and Celecoxib group. In the test prostanoids, nitrate and nitrite were measured by gas chromatograpy/tandem-mass-spectrometry (GC-MS/MS) in 24-hours-collected urine. Additionally we measured cholesterol and triglycerides in plasma. The aortas of the examinated animals were measured optically using a planimetrical method. The measurement of prostanoids, isoprostanes, nitrate and nitrite showed considerable variations and particulary significant differences (p < 0.01) even in the initial values. By the treatment with Celecoxib the rate of atherosclerosis was reduced in a highly significant way in comparison to the cholesterol group and the DHEA-group. Consequently the test demonstrated a significant role of COX-2 in the development of atherogenesis.展开更多
基金Supported by Grants from the Project of Beijing University of Chinese Medicine in China:Studies on Effect of Electroacupuncture at Different Acupoint Modules in the Rat Model Lumbar Disc Herniation By COX2-PGE2 Pathway and Mechanisms of Acupoints Compatibility(No.JYB22-JS022)
文摘OBJECTIVE: To observe the effect of electroacupuncture(EA) treatment on the expression of E-prostanoid 2(EP2) in the spinal cord using a rat model of neuropathic pain, and to examine the effect of different acupuncture prescriptions.METHODS: Rats were randomly divided into six groups: a normal group, model group, sham group,EA 1 group(distal-proximal acupoints), EA 2 group(proximal acupoints), and EA 3 group(distal acupoints). Rats in the EA groups were treated for20 min, once daily for 7 days. The mechanical withdrawal threshold was evaluated at 1 day preoperatively and at 3, 5, and 7 days postoperatively. At 7days postoperatively, hematoxylin-eosin(HE) staining was used to investigate spinal morphological changes. Spinal EP2 messenger ribonucleic acid(m RNA) was detected using reverse-transcription polymerase chain reaction.RESULTS: After the EA treatment, the mechanical withdrawal threshold was up-regulated compared with the model group(P < 0.05). The expression of EP2 m RNA was up-regulated in the spinal cord on day 7 after surgery(P < 0.05). EA stimulation tended to down-regulate EP2 m RNA expression compared with the model group(P > 0.05). The EA 1and EA 2 groups showed a larger treatment effect than the EA 3 group. The HE results showed that EA can improve spinal histomorphology induced by neuropathic pain.CONCLUSION: EA had a strong analgesic and anti-inflammatory effect. The therapeutic effect of EA on the down-regulation of spinal EP2 m RNA expression may be greater when either local acupoints or a distal-proximal combination of acupoints are used than when distal points are used.
基金the Ministry of Health for the financial support of China(No.94-2-025).
文摘A new method for introduction to-side chain of prostanoid was described in this note. Starting from acid chloride （3）, via Barton radical reaction, a trans α,β-unsaturated ketone sython was introduced.
文摘Many agents are known to cause qualitative and quantitative differences in intrarenal blood flow. This study tested the hypothesis that angiotensin II (AII) evokes a differential effect on cortical (CBF) and medullary blood flow (MBF) and that AT2 receptor mediates AII-induced increase in renal MBF by mechanisms related to nitric oxide (NO) and prostanoids. AII (100, 300 and 1000 ng/kg/min) increased mean arterial blood pressure (MABP) by 24% ± 7% (p G nitro-L-arginine (L-NNA), an inhibitor of NO synthase (100 mg/L in drinking water) enhanced AII effects on MABP (169 ± 75, p ATP channel blocker, did not affect intra-renal hemodynamics elicited by AII. Blockade of AT2 receptors with PD123319 (50 μg/kg/min) did not change basal or AII-induced changes MABP or CBF but blunted AII-induced increase in MBF by 60% ± 11 % (p 2 receptor agonist, elicited a reduction in MABP and increases in CBF and MBF that were abolished or attenuated by PD123319. These findings demonstrate that AII elicited differential changes in intrarenal blood flow;an AT1-mediated reduction in CBF but an AT2-mediated increase in MBF. The AT2 receptor-mediated increase in MBF involves guanylase cyclase, NO and dilator prostanoids but not KATP channels.
文摘A stereoselective and regiospecific synthesis of procursors(2),(4),(6)and(7)of prostacyclin analogues from 2,3-epoxylbicyclo[3.2.0]hept-6-one(1)are described.
文摘Background Cyclooxygenase （COX） is the rate-limiting enzyme in the production of prostanoids from arachidonic acid. COX-2 is the inducible enzyme in the COX family, together with the prostanoids forms the COX-2/prostanoid pathway. Research showed that the COX-2/prostanoid pathway is activated in hepatic diseases and liver stress reaction, such as fibrogenesis, portal hypertension, carcinogenesis, and ischemic/repeffusion injury. But there was no report on visceral pain induced liver stress. This study was to investigate the role of the COX-2/prostanoid pathway in liver stress response in rat acute colitis visceral pain liver stress model.Methods Fifty-three male SD rats were randomly divided into Naive, Model, NS398 treatment, and Morphine treatment groups. The rat acute colitis visceral pain liver stress model was established under anesthesia by the colonic administration of 0.5 ml of 6% acetic acid using a urethral catheter. NS398 and morphine were administrated 30 minutes prior to model establishment in NS398 and Morphine treatment groups respectively. Spontaneous activities and pain behavior were counted and the extent of colonic inflammation was assessed histologically. Liver tissue levels of Glutathione-S-Transferase （GST） activity, COX-2 mRNA, prostaglandin E2 （PGE2）, thromboxane B2 （TXB2） and 6-Ketone-prostaglandin F1α （6-K-PGF1α） contents were assessed.Results Thirty minutes after the colonic administration of acetic acid, a significant decrease in spontaneous activities and an increase in pain behaviors were observed in Model group （P〈0.01 and P〈0.05 respectively）, accompanied by colonic inflammation. Liver GST activity levels significantly dropped （P〈0.05）. Liver COX-2 mRNA expressi.on significantly increased, accompanied by an increase in liver concentrations of PGE2 and TXB2, but no obvious change in 6-K-PGF1α concentrations. NS398 and morphine both ameliorated post-stress liver GST activity （P〈0.05 and P〈0.01 respectively）, decreased stress-induced COX-2 expression, decreased PGE2 and TXB2 production, but increased liver 6-K-PGF1α levels. Morphine attenuation in colonic tissue inflammation was apparent at 24 hours （P〈0.05）.Conclusions Acute colitis visceral pain liver stress can induce liver injury. Liver injury might have occurred through the activation of the COX-2/prostanoid pathway and increased production of PGE2 and TXB2. Effective analgesia might offer protective effect during visceral pain stress.
文摘Atherosclerosis is the most prevalent disease in middle and later years of human life. Heart attacks and strokes are among the most frequent causes of death. New approaches in therapy are the use of NSAID’s (nonsteroidal antiphlogistical drugs) of the new generation (selective inhibitors of COX-2) and DHEA (Dehydroepiandrostenon). The key enzyme of prostaglandin synthesis, the COX-2 isoenzyme, is predominantly found in inflammatory tissue. Out of this results a possible importance of COX-2-inhibitors in prophylaxis of atherosclerosis. Our study intended to examine the significance of COX-2 and the COX-2-formed prostanoids, as well as the significance of COX-2-independent iso-prostanes on atherosclerosis. For that purpose we tested the effect of the selective COX-2-inhibitor Celecoxib on rabbits fed with cholesterol and compared this with the effect of the steroid hormone DHEA in 4 groups: healthy control, cholesterol-fed control, DHEA-group and Celecoxib group. In the test prostanoids, nitrate and nitrite were measured by gas chromatograpy/tandem-mass-spectrometry (GC-MS/MS) in 24-hours-collected urine. Additionally we measured cholesterol and triglycerides in plasma. The aortas of the examinated animals were measured optically using a planimetrical method. The measurement of prostanoids, isoprostanes, nitrate and nitrite showed considerable variations and particulary significant differences (p < 0.01) even in the initial values. By the treatment with Celecoxib the rate of atherosclerosis was reduced in a highly significant way in comparison to the cholesterol group and the DHEA-group. Consequently the test demonstrated a significant role of COX-2 in the development of atherogenesis.
