ABSTRACT
Objective To observe the effect of microinjection of oxytocin(OT) into paraventricular nucleus(PVN) on gastric ischemia-reperfusion(GI-R) injury and its molecular mechanism.Methods GI-R injury was induced in rats by clamping the celiac artery for 30 min and followed by reperfusing for 1 h.A cannula was inserted into the unilateral PVN for microinjection of OT.The gastric mucosal injury index was counted grossly.The expressions of Akt and caspase-3 in rat gastric mucosa were examined by Western blot and by immunohistochemistry.Results Microinjection of OT into PVN dose-dependently allevated gastric mucosal injury subjected to GI-R.Microinjection OT into PVN significantly increased the expression of Akt protein and decreased the level of caspase-3 in gastric mucosal following GI-R.The effects of OT were prevented by pretreatment with OT receptor antagonist atosiban into the lateral cerebral ventricle.Conclusion Microinjection of OT into PVN significantly protected against GI-R injury.These effects of OT are mediated by its receptors.The mechanisms are mediated by increasing Akt expression,which in turn inhibits caspase-3 expression.
ABSTRACT
Objective To observe effects of Apelin-13 microinjection into the hypothalamic paraventricular nucleus(PVN) on gastric ischemia-reperfusion(GI-R) injury in rats.Methods After Apelin-13 injection into PVN,the experimental model of GI-R was established by clamping the celiac artery for 30 min and then reperfused the artery for 1 h.We used immunohistochemistry to detect the gastric mucosal cells apoptosis,proliferation and the expression of BCL-2,BAX.Results(1)Apelin-13 microinjection into the PVN aggravated GI-R injury in an dose-dependent manner with dosages as 0.2,1.0 or 5.0 ?g,respectively.(2)Compared with GI-R group,Apelin-13 microinjection into PVN markedly increased gastric mucosal cellular apoptosis,decreased the proliferation and promoted protein expression of BAX,but obviously inhibited the protein expression of BCL-2.Conclusion Apelin-13 microinjection into the PVN may aggravate GI-R injury by promoting gastric mucosal cellular apoptosis and inhibiting proliferation.
ABSTRACT
Objective To observe the effects of electrical stimulation of paraventricular nucleus(PVN) on gastric mucosal cellular apoptosis,proliferation,and expression of BCL-2,BAX induced by gastric ischemia-reperfusion(GI-R) and the potential mechanisms of protection of PVN on GI-R injury.Methods After electrical stimulation of PVN,the experimental model of GI-R were established by clamping the celiac artery for 30 min and then reperfusing the artery for 30 min,1 h,3 h,or 6 h respectively.We used immunohistochemistry to detect the gastric mucosal cells apoptosis,proliferation and the expression of BCL-2,BAX.Results Compared with GI-R group,the electrical stimulation of PVN markedly decreased gastric mucosal cellular apoptosis,increased the proliferation,and promoted the protein expression of BCL-2,but markedly inhibited the protein expression of BAX at 30 min,1 h,3 h after reperfusion respectively.Conclusion The protective effect of PVN on GI-R injury is associated with up-regulation of expression of BCL-2 and down-regulation expression of BAX,and so inhibited gastric mucosal cellular apoptosis and promoted proliferation.