摘要
目的 :观察还原型谷胱甘肽(reduced glutathione hormone,GSH)对重症急性胰腺炎(severe acute pancreatitis,SAP)大鼠海马神经元的保护作用。方法:72只SD大鼠分为3组:生理盐水组(NS组)、SAP组和GSH组,每组又分为3、6、12 h 3个亚组。SAP组以5%牛磺胆酸钠逆行注入大鼠胰胆管建立SAP模型,NS组仅向胰胆管注射与SAP组等量的无菌生理盐水,GSH组在造模后按每100 g体重腹腔内注射25 mg GSH。分别采用尼氏染色检测大鼠脑组织海马区神经元损伤情况,TUNEL法检测海马神经元凋亡情况,免疫组化法检测海马组织NF-κB p65的表达。结果:与SAP组比较,GSH组在GSH治疗后3、6 h,胰腺病理评分明显改善(P均<0.05),海马神经元凋亡指数明显下降(P均<0.05)。海马NF-κB p65表达受抑,尤以GSH组GSH治疗6 h后明显。结论:GSH在SAP脑损伤的早、中期可以通过抑制大鼠海马组织NF-k B p65蛋白的表达来减轻神经元凋亡。
Objective：To investigate the protective effect of reduced glutathione（GSH） on the hippocampal neuron of rats with severe acute pancreatitis（SAP）. Methods：Seventy-two SD rats were equally assigned into 3 groups：the normal saline（NS） group,the SAP group and the GSH group. Each group included 3 subgroups：the 3,6 and 12 h groups. SAP models were established by retrograde injection of 5% sodium taurocholate into the bile-pancreatic duct. Rats in the NS group were injected with normal saline instead of sodium taurocholate. Rats in the GSH group were peritoneally injected with GSH at the dosage of 25 mg / 100 g body weight. Nissle stain was performed to evaluate the severity of brain injury. Hippocampal neuronal apoptosis was detected by TUNEL,and NF-κB p65 expression was detected by immunohistochemistry. Results：Pathological scores of pancreatic injury were significantly lower in the groups of GSH（3 h） and GSH（6 h） than those in the groups of SAP（3 h） and SAP（6 h）（P〈0.05）. Hippocampal neuronal apoptosis indexes were significantly decreased（P〈0.05）. The expression of NF-κB p65 was depressed mainly in the GSH（6 h）group.Conclusion：The hippocampal neuronal apoptosis in SAP rats with brain injury is reduced by GSH through an inhibition of NF-κB p65 expression in the hippocampus.
出处
《南京医科大学学报（自然科学版）》
CAS
CSCD
北大核心
2016年第3期298-301,共4页
Journal of Nanjing Medical University(Natural Sciences)
基金
南通市社会发展指导性计划(S11950)
