AIM:To investigate the relation of reactive oxygen species (ROS) to hypoxia induced factor 1α (HIF-1α) in gastric ischemia. METHODS:The animal model of gastric ischemia reperfusion was established by placing an elas...AIM:To investigate the relation of reactive oxygen species (ROS) to hypoxia induced factor 1α (HIF-1α) in gastric ischemia. METHODS:The animal model of gastric ischemia reperfusion was established by placing an elastic rubber band on the proximal part of the bilateral lower limb for ligature for 3 h and reperfusion for 0,1,3,6,12 or 24 h. Ischemic post-conditioning,three cycles of 30-s reperfusion and 30-s femoral aortic reocclusion were conducted before reperfusion. Histological and immunohistochemical methods were used to assess the gastric oxidative damage and the expression of HIF1-α in gastric ischemia. The malondialdehyde (MDA) content and superoxide dismutase (SOD),xanthine oxidase (XOD) and myeloperoxidase (MPO) activities were determined by colorimetric assays. RESULTS:Ischemic post-conditioning can reduce post-ischemic oxidative stress and the expression of HIF-1α of gastric tissue resulting from limb ischemia reperfusion injury. MDA,SOD,XOD and MPO were regarded as indexes for mucosal injuries from ROS,and ROS was found to affect the expression of HIF-1α under gastric ischemic conditions. CONCLUSION:ROS affects HIF-1α expression under gastric ischemic conditions induced by limb ischemia reperfusion injury. Therefore,ROS can regulate HIF-1α expression in gastric ischemia.展开更多
Endoscopic epinephrine injection is relatively easy,quick and inexpensive.Furthermore,it has a low rate of com-plications,and it is widely used for the management of nonvariceal upper gastrointestinal bleeding.There h...Endoscopic epinephrine injection is relatively easy,quick and inexpensive.Furthermore,it has a low rate of com-plications,and it is widely used for the management of nonvariceal upper gastrointestinal bleeding.There have been several case reports of gastric ischemia after en-doscopic injection therapy.Inadvertent intra-arterial in-jection may result in either spasm or thrombosis,leading to subsequent tissue ischemia or necrosis,although the stomach has a rich vascular supply and the vascular reserve of the intramural anastomosis.In addition to endoscopic injection therapy,smoking,hypertension and atherosclerosis are risk factors of gastric ischemia. We report a case of gastric ischemia after submucosal epinephrine injection in a 51-year-old woman with hy-pertension and liver cirrhosis.展开更多
Background We investigated the role in electrical stimulations of paraventricular nucleus （PVN） on gastric mucosal cells and the activity of mitogen-activated protein kinases （MAPKs） family members induced by gast...Background We investigated the role in electrical stimulations of paraventricular nucleus （PVN） on gastric mucosal cells and the activity of mitogen-activated protein kinases （MAPKs） family members induced by gastric ischemia-reperfusion （GI-R）. And we elucidated the molecular mechanisms of the protection of PVN from GI-R injuries. Methods Sprague-Dawley rats were divided randomly into 4 groups： Group I, the sham-operated GI-R control group; Group II, the sham-operated electrical stimulations to PVN ＋ sham-operated GI-R control group; Group III, the GI-R group; and Group IV, the electrical stimulations to PVN ＋ GI-R group. In all of the experiments, the PVN was stimulated prior to the induction of GI-R. The GI-R model was established by clamping the celiac artery for 30 minutes to induce ischemia and then was released to allow reperfusion for 30 minutes, 1 hour, 3 hours and 6 hours, respectively. The gastric mucosal cellular apoptosis, proliferation, and the expression and activity of MAPKs protein were observed by immunohistochemistry and Western blotting, respectively. Results Compared with the GI-R group, the application of electrical stimulations in the PVN significantly depressed gastric mucosal cellular apoptosis and enhanced gastric mucosal cellular proliferation following the 30-minute, 1-hour and 3-hour intervals of reperfusion; it also promoted the activation of p-ERK during the early phase of reperfusion but inhibited the activation of p-JNK1/2 and p-p38 following the 30-minute, 1-hour and 3-hour intervals of reperfusion. Conclusions The protection of PVN against GI-R injuries may attribute to the inhibition of apoptosis and the promotion of the proliferation of gastric mucosal cells during GI-R. This protective effect is mediated by activating the ERK pathway and depressing the JNK, the JNK. p38 MAPK oathwavs of the oastric mucosal cells.展开更多
AIM: To investigate the effects of electrical stimulation of hypothalamic paraventricular nuclei (PVN) on gastric mucosal cellular apoptosis and proliferation induced by gastric ischemia/reperfusion (I/R) injury. METH...AIM: To investigate the effects of electrical stimulation of hypothalamic paraventricular nuclei (PVN) on gastric mucosal cellular apoptosis and proliferation induced by gastric ischemia/reperfusion (I/R) injury. METHODS: For different experimental purposes, stimulating electrode plantation or electrolytic destruction of the PVN was applied, then the animals' GI/R injury model was established by clamping the celiac artery for 30min and allowing reperfusing the artery for 30min, 1h, 3h or 6h respectively. Then histological, immunohistochemistry methods were used to assess the gastric mucosal damage index, the gastric mucosal cellular apoptosis and proliferation at different times. RESULTS: The electrical stimulation of PVN significantly attenuated the GI/R injury at 30 min, 1h and 3h after reperfusion. The electrical stimulation of PVN decreased gastric mucosal apoptosis and increased gastric mucosal proliferation. The electrolytic destruction of the PVN could eliminate the protective effects of electrical stimulation of PVN on GI/R injury. These results indicated that the PVN participated in the regulation of GI/R injury as a specific area in the brain, exerting protective effects against the GI/R injury, and the protection was associated with the inhibition of cellular apoptosis and the promotion of gastric mucosal proliferation. CONCLUSION: Stimulating PVN significantly inhibits the gastric mucosal cellular apoptosis and promots gastric mucosal cellular proliferation. This may explain the protective mechanisms of electrical stimulation of PVN against GI/R injury.展开更多
AIM:To investigate the protective effects of remote ischemic postconditioning(RIP)against limb ischemiareperfusion(IR)-induced gastric mucosal injury.METHODS:Gastric IR was established in male Wistar rats by placing a...AIM:To investigate the protective effects of remote ischemic postconditioning(RIP)against limb ischemiareperfusion(IR)-induced gastric mucosal injury.METHODS:Gastric IR was established in male Wistar rats by placing an elastic rubber band under a pressure of 290-310 mmHg on the proximal part of both lower limbs for 3 h followed by reperfusion for 0,1,3,6,12or 24 h.RIP was performed using three cycles of 30 s of reperfusion and 30 s of reocclusion of the femoral aortic immediately after IR and before reperfusion for up to 24 h.Rats were randomly assigned to receive IR(n=36),IR followed by RIP(n=36),or sham treatment(n=36).Gastric tissue samples were collected from six animals in each group at each timepoint and processed to determine levels of malondialdehyde(MDA),superoxide dismutase(SOD),xanthine oxidase(XOD)and myeloperoxidase(MPO).Additional samples were processed for histologic analysis by hematoxylin and eosin staining.Blood samples were similarly collected to determine serum levels of lactate dehydrogenase(LDH),creatine kinase(CK),tumor necrosis factor(TNF)-αand interleukin(IL)-10.RESULTS:The pathologic changes in gastric tissue induced by IR were observed by light microscopy.Administration of RIP dramatically reduced the gastric damage score after 6 h of reperfusion(5.85±0.22 vs7.72±0.43;P<0.01).In addition,RIP treatment decreased the serum activities of LDH(3.31±0.32 vs 6.46±0.03;P<0.01),CK(1.94±0.20 vs 4.54±0.19;P<0.01)and the concentration of TNF-α(53.82±0.85vs 88.50±3.08;P<0.01),and elevated the concentration of IL-10(101.46±5.08 vs 99.77±4.32;P<0.01)induced by IR at 6 h.Furthermore,RIP treatment prevented the marked elevation in MDA(3.79±0.29vs 6.39±0.81)content,XOD(7.81±0.75 vs 10.37±2.47)and MPO(0.47±0.05 vs 0.82±0.03)activities,and decrease in SOD(4.95±0.32 vs 3.41±0.38;P<0.01)activity in the gastric tissue as measured at 6 h.CONCLUSION:RIP provides effective functional protection and prevents cell injury to gastric tissue induced by limb IR via anti-inflammatory and antioxidant actions.展开更多
基金Supported by Technology from the School of Basic Medical Sciences of Lanzhou University and the Animal Experimental Center, Gansu College of Traditional Chinese Medicine
文摘AIM:To investigate the relation of reactive oxygen species (ROS) to hypoxia induced factor 1α (HIF-1α) in gastric ischemia. METHODS:The animal model of gastric ischemia reperfusion was established by placing an elastic rubber band on the proximal part of the bilateral lower limb for ligature for 3 h and reperfusion for 0,1,3,6,12 or 24 h. Ischemic post-conditioning,three cycles of 30-s reperfusion and 30-s femoral aortic reocclusion were conducted before reperfusion. Histological and immunohistochemical methods were used to assess the gastric oxidative damage and the expression of HIF1-α in gastric ischemia. The malondialdehyde (MDA) content and superoxide dismutase (SOD),xanthine oxidase (XOD) and myeloperoxidase (MPO) activities were determined by colorimetric assays. RESULTS:Ischemic post-conditioning can reduce post-ischemic oxidative stress and the expression of HIF-1α of gastric tissue resulting from limb ischemia reperfusion injury. MDA,SOD,XOD and MPO were regarded as indexes for mucosal injuries from ROS,and ROS was found to affect the expression of HIF-1α under gastric ischemic conditions. CONCLUSION:ROS affects HIF-1α expression under gastric ischemic conditions induced by limb ischemia reperfusion injury. Therefore,ROS can regulate HIF-1α expression in gastric ischemia.
文摘Endoscopic epinephrine injection is relatively easy,quick and inexpensive.Furthermore,it has a low rate of com-plications,and it is widely used for the management of nonvariceal upper gastrointestinal bleeding.There have been several case reports of gastric ischemia after en-doscopic injection therapy.Inadvertent intra-arterial in-jection may result in either spasm or thrombosis,leading to subsequent tissue ischemia or necrosis,although the stomach has a rich vascular supply and the vascular reserve of the intramural anastomosis.In addition to endoscopic injection therapy,smoking,hypertension and atherosclerosis are risk factors of gastric ischemia. We report a case of gastric ischemia after submucosal epinephrine injection in a 51-year-old woman with hy-pertension and liver cirrhosis.
基金grants from the National Natural Science Foundation of China(No.30370533and30570671)Educational Department Science Research Foundation of Jiangsu Province(No. 05KJB310134)
文摘Background We investigated the role in electrical stimulations of paraventricular nucleus （PVN） on gastric mucosal cells and the activity of mitogen-activated protein kinases （MAPKs） family members induced by gastric ischemia-reperfusion （GI-R）. And we elucidated the molecular mechanisms of the protection of PVN from GI-R injuries. Methods Sprague-Dawley rats were divided randomly into 4 groups： Group I, the sham-operated GI-R control group; Group II, the sham-operated electrical stimulations to PVN ＋ sham-operated GI-R control group; Group III, the GI-R group; and Group IV, the electrical stimulations to PVN ＋ GI-R group. In all of the experiments, the PVN was stimulated prior to the induction of GI-R. The GI-R model was established by clamping the celiac artery for 30 minutes to induce ischemia and then was released to allow reperfusion for 30 minutes, 1 hour, 3 hours and 6 hours, respectively. The gastric mucosal cellular apoptosis, proliferation, and the expression and activity of MAPKs protein were observed by immunohistochemistry and Western blotting, respectively. Results Compared with the GI-R group, the application of electrical stimulations in the PVN significantly depressed gastric mucosal cellular apoptosis and enhanced gastric mucosal cellular proliferation following the 30-minute, 1-hour and 3-hour intervals of reperfusion; it also promoted the activation of p-ERK during the early phase of reperfusion but inhibited the activation of p-JNK1/2 and p-p38 following the 30-minute, 1-hour and 3-hour intervals of reperfusion. Conclusions The protection of PVN against GI-R injuries may attribute to the inhibition of apoptosis and the promotion of the proliferation of gastric mucosal cells during GI-R. This protective effect is mediated by activating the ERK pathway and depressing the JNK, the JNK. p38 MAPK oathwavs of the oastric mucosal cells.
基金grants from the National Natural Science Foundation of China, No. 30370533, 30570671the Educational Department Science Research Foundation of Jiangsu Province, No. 99KJB310005,05KJB310134
文摘AIM: To investigate the effects of electrical stimulation of hypothalamic paraventricular nuclei (PVN) on gastric mucosal cellular apoptosis and proliferation induced by gastric ischemia/reperfusion (I/R) injury. METHODS: For different experimental purposes, stimulating electrode plantation or electrolytic destruction of the PVN was applied, then the animals' GI/R injury model was established by clamping the celiac artery for 30min and allowing reperfusing the artery for 30min, 1h, 3h or 6h respectively. Then histological, immunohistochemistry methods were used to assess the gastric mucosal damage index, the gastric mucosal cellular apoptosis and proliferation at different times. RESULTS: The electrical stimulation of PVN significantly attenuated the GI/R injury at 30 min, 1h and 3h after reperfusion. The electrical stimulation of PVN decreased gastric mucosal apoptosis and increased gastric mucosal proliferation. The electrolytic destruction of the PVN could eliminate the protective effects of electrical stimulation of PVN on GI/R injury. These results indicated that the PVN participated in the regulation of GI/R injury as a specific area in the brain, exerting protective effects against the GI/R injury, and the protection was associated with the inhibition of cellular apoptosis and the promotion of gastric mucosal proliferation. CONCLUSION: Stimulating PVN significantly inhibits the gastric mucosal cellular apoptosis and promots gastric mucosal cellular proliferation. This may explain the protective mechanisms of electrical stimulation of PVN against GI/R injury.
基金Supported by Lanzhou City Science and Technology Development Plan,No.2009-1-52
文摘AIM:To investigate the protective effects of remote ischemic postconditioning(RIP)against limb ischemiareperfusion(IR)-induced gastric mucosal injury.METHODS:Gastric IR was established in male Wistar rats by placing an elastic rubber band under a pressure of 290-310 mmHg on the proximal part of both lower limbs for 3 h followed by reperfusion for 0,1,3,6,12or 24 h.RIP was performed using three cycles of 30 s of reperfusion and 30 s of reocclusion of the femoral aortic immediately after IR and before reperfusion for up to 24 h.Rats were randomly assigned to receive IR(n=36),IR followed by RIP(n=36),or sham treatment(n=36).Gastric tissue samples were collected from six animals in each group at each timepoint and processed to determine levels of malondialdehyde(MDA),superoxide dismutase(SOD),xanthine oxidase(XOD)and myeloperoxidase(MPO).Additional samples were processed for histologic analysis by hematoxylin and eosin staining.Blood samples were similarly collected to determine serum levels of lactate dehydrogenase(LDH),creatine kinase(CK),tumor necrosis factor(TNF)-αand interleukin(IL)-10.RESULTS:The pathologic changes in gastric tissue induced by IR were observed by light microscopy.Administration of RIP dramatically reduced the gastric damage score after 6 h of reperfusion(5.85±0.22 vs7.72±0.43;P<0.01).In addition,RIP treatment decreased the serum activities of LDH(3.31±0.32 vs 6.46±0.03;P<0.01),CK(1.94±0.20 vs 4.54±0.19;P<0.01)and the concentration of TNF-α(53.82±0.85vs 88.50±3.08;P<0.01),and elevated the concentration of IL-10(101.46±5.08 vs 99.77±4.32;P<0.01)induced by IR at 6 h.Furthermore,RIP treatment prevented the marked elevation in MDA(3.79±0.29vs 6.39±0.81)content,XOD(7.81±0.75 vs 10.37±2.47)and MPO(0.47±0.05 vs 0.82±0.03)activities,and decrease in SOD(4.95±0.32 vs 3.41±0.38;P<0.01)activity in the gastric tissue as measured at 6 h.CONCLUSION:RIP provides effective functional protection and prevents cell injury to gastric tissue induced by limb IR via anti-inflammatory and antioxidant actions.
