RÉSUMÉ
Objective:To explore the feature of FOS expression in oxytocin-and vasopressin-positive neurons in the hypothalamic paraventricular nucleus(PVN)under different status of diabetes mellitus(DM).Methods:Intraperito-neal injection of vehicle or STZ in mice was conducted to establish control or diabetes model.Mechanical sensitivity was evaluated by von Frey filament tests to distinguish diabetic neuropathic pain(DNP)from without-pain group(DWP).The expression of FOS,oxytocin(OXT)-and vasopressin(VP)-positive neurons,as well as their double labeling was detected by immunohistochemical and immunofluorescent staining.Cell counting and comparison were made in groups.Results:FOS expression was easily detected in the PVN in the three groups(Control group,DNP group and DWP group)at 7 days,while that in DWP and DNP groups at 28 days was hardly detectable,with the number being signifi-cantly different from the 7 days group(P＜0.05 or 0.001).Likewise,compared with the control group,immunofluo-rescent signals for VP and OXT staining in the DNP and DWP groups also showed a trend of weakening as the modeling time increased(P＜0.05).The cell counting after double staining for VP or OXT with FOS showed that,in the DWP group at 7 days,the number of VP and FOS double-labeled neurons was 74.33±22.10,accounting for(56.64± 7.52)％of VP-positive cells,whereas the double labeling rate for OXT and FOS was only(10.44±3.14)％.In the DNP group at 7 days,the number of OXT and FOS double-labeled neurons was 51.00±31.80,accounting for(18.50 ±9.51)％of OXT-positive neurons,whereas the double labeling rate for VP and FOS was only(9.34±3.27)％.In contrast to these changes in 7 days group,the expression of FOS decreased sharply in the group of 28 days,thereby al-most no double-labeled neurons.Conclusion:The plasticity changes of oxytocin-and vasopressin-positive neurons in the PVN are different depending on the status of pain and non-pain,and the stage of disease progression.Understanding the changes is of great significance for unravelling the neural mechanism of diabetes and its complications.
RÉSUMÉ
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.
RÉSUMÉ
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.