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Objective To investigate the effect of fluvastatin on the expressions of caspase-12,CCAAT/enhancer-binding protein homologous protein(CHOP), and c-Jun N-terminal kinases (JNK) in ischemia-reperfusion brain injury in rats.Methods Forty two rats were randomly divided into sham operation group (6 rats), ischemia-reperfusion (I/R) group (18 rats), and fluvastatin (Flu) group (18 rats).The rats of I/R and Flu groups were molded by modified Longa intraluminal thread, then put to death at 2 h occlusion and 24 h reperfusion point.Expressions of caspase-12, CHOP, and JNK were detected with immunohistochemistry and Western blot.Results Immunohistochemistry and Western blot showed that the expressions of caspase-12, CHOP, and JNK were increased at 24 h reperfusion.Compared to I/R group, the expressions of caspase-12 and CHOP in Flu group were decreased significantly (all P ＜0.01);and the expression of JNK had no difference between I/R and Flu groups(P ＞ 0.05).Conclusions The increased expression of caspase-12, CHOP, and JNK showed that endoplasmic reticulum stress was involved in the pathological process of ischemia-reperfusion brain injury.Fluvastatin could inhibit the expression of caspase12 and CHOP, and could delete endoplasmic reticulum stress (ERS) in ischemia-reperfusion brain injury.
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Objective To investigate the protective effect of meglumine adenosine cyclosphosp (MAC) on the cerebral ischemia-reperfusion (I/R) injury in rabbits.Methods Twenty four healthy rabbits were randomly divided into control group (n =6),I/R group (n =6),MAC pretreated group (n =6),and MAC treated group (n =6).Cerebral ischemia-reperfusion injury model was made by separating and electrocoagulating vertebral arteries and clipping common carotid arteries in the latter 3 groups after anesthesia.The sham-operated group underwent vessel separation without clipping.L/R group was administered with nothing,while MAC pretreated group with MAC before ischemia,and MAC treated group with MAC just after ischemia.Blood was gathered from jugular vein before ischemia,and 30 min,1 h,and 2 h after reperfusion for testing IL-8,superoxide dismutase (SOD) and malondialdehyde (MDA).The brain tissue slice was observed by optical microscope.Results Compared to control group and before ischemia,the levels of IL-8 and SOD in serum were significantly increased and decreased,and the levels of MDA was significantly increased at 30 min after reperfusion in I/R group; the levels of IL-8 and MDA in serum were significantly increased,and the levels of SOD in serum was significantly decreased at 1 h and 2 h after reperfusion in I/R group.The levels of IL-8 in serum was less at 30 min and 1 h and 2 h after reperfusion in MAC pretreated group than in I/R group.At 1 h and 2 h after reperfusion,the levels of MDA in serum was less and the levels of SOD in serum was higher in MAC pretreated group than in I/R group.At 1 h and 2 h after reperfusion,the levels of IL-8 in serum were less and the levels of SOD in serum were higher in MAC treated group than in I/R group.The levels of MDA in serum were less at 2 h after reperfusion in MAC treated group than in I/R group.Compared to I/R group,pathological change was lighter in the MAC pretreated and MAC treated group.Conclusions MAC has a fine cerebral-protective effect and has no side effect.