Abstract：Objective To investigate the effects of apigenin combined with ischemic postconditioning on renal ischemia/reperfusion injury in rats. Methods Fifty rats were randomly divided into 5 groups: sham-operated group (sham group), ischemia/reperfusion group (I/R group), apigenin group (api group), ischemic postconditioning group (IPO group) and api+IPO group. The rat model with renal ischemia/reperfusion injury was established, then the animals were sacrificed and nephridial tissue was taken to make paraffin-embedded sections. The pathologic changes of nephridial tissue were observed, the expression of Fas, Caspase-3, Bax were detected by immunohistochemistry, the expression of Fas, Caspase-3, PARP-1 and Bcl-2 were detected by real-time PCR, the expression of Caspase-3, Bax and Bcl-2 were detected by Western blot. Results Compared with the sham group, in I/R group, the pathological tissue showed that kidney tubules were damaged seriously; the immunohistochemistry showed that the expression of Fas and Caspase-3 were enhanced, the expression of Bcl-2 was decreased (P ＜ 0.01); Real-time PCR showed that the expression of Fas, Caspase-3 and PARP-1 mRNA were up-regulated significantly, the expression of Bcl-2 was down-regulated significantly (P ＜ 0.01); Western blot showed that the expression of Caspase-3 and Bax were increased significantly, the expression of Bcl-2 was reduced significantly, the differences were highly statistically significant (P ＜ 0.01). Compared with I/R group, in api+I/R group, IPO group and api+IPO group, the pathological tissue showed that kidney tubules were alleviated; the immunohistochemistry showed that the expression of Fas and Caspase-3 were reduced, the expression of Bcl-2 was increased (P ＜ 0.05); Real-time PCR showed that the expression of Fas, Caspase-3 and PARP-1 mRNA were down-regulated significantly, the expression of Bcl-2 was up-regulated significantly (P ＜ 0.05); Western blot showed that the expression of Caspase-3 and Bax were reduced significantly, the expression of Bcl-2 was increased significantly, the differences were statistically significant (P ＜ 0.05). Conclusion Both apigenin and ischemic postconditioning can reduce the renal ischemia/reperfusion injury, the mechanism may be related to up-regulating the expression of Bcl-2 and down-regulating the expression of Bax, Caspase-3, so as to inhibit the cell apoptosis caused by renal ischemia/reperfusion injury.
刘洋 刘修恒 王磊 杜洋 汪志顺 陈志远 郭佳. 芹黄素联合缺血后处理对大鼠肾缺血再灌注损伤的影响[J]. 中国医药导报, 2017, 14(15): 22-25.
LIU Yang LIU Xiuheng WANG Lei DU Yang WANG Zhishun CHEN Zhiyuan GUO Jia . Effects of apigenin combined with ischemic postconditioning on renal ischemia/reperfusion injury in rats. 中国医药导报, 2017, 14(15): 22-25.
[1] Azari O，Kheirandish R，Azizi S，et al. Protective Effects of Hydrocortisone，Vitamin C and E Alone or in Combination against Renal Ischemia-Reperfusion Injury in Rat [J]. Iran J Pathol，2015，10（4）：272-280.
[2] Asghari A，Takhtfooladi MA，Hoseinzadeh HA. Effect of photobiomodulation on ischemia/reperfusion-induced renal damage in diabetic rats [J]. Lasers Med Sci，2016，31（9）：1943-1948.
[3] Zhu J，Yao K，Wang Q，et al. Ischemic Postconditioning-Regulated miR-499 Protects the Rat Heart Against Ischemia/Reperfusion Injury by Inhibiting Apoptosis through PDCD4 [J]. Cell Physiol Biochem，2016，39（6）：2364-2380.
[4] Guo Q，Du X，Zhao Y，et al. Ischemic postconditioning prevents renal ischemia reperfusion injury through the induction of heat shock proteins in rats [J]. Mol Med Rep，2014，10（6）：2875-2881.
[5] Xia A，Li Y，Li N，et al. Roles of MAPKAPK-2 and HSP27 in the reduction of renal ischemia-reperfusion injury by ischemic postconditioning in rats [J]. Int Urol Nephrol，2014，46（7）：1455-1464.
[6] Luan RL，Meng XX，Jiang W. Protective Effects of Apigenin Against Paraquat-Induced Acute Lung Injury in Mice [J]. Inflammation，2016，39（2）：752-758.
[7] Qin Y，Zhao D，Zhou HG，et al. Apigenin inhibits NF-kappaB and snail signaling，EMT and metastasis in human hepatocellular carcinoma [J]. Oncotarget，2016，7（27）：41421-41431.
[8] Tanaka R，Yazawa M，Morikawa Y，et al. Sex differences in ischaemia/reperfusion-induced acute kidney injury depends on the degradation of noradrenaline by monoamine oxidase [J]. Clin Exp Pharmacol Physiol，2017，44（3）：371-377.
[9] Liou CM，Tsai SC，Kuo CH，et al. Cardiac Fas-dependent and mitochondria-dependent apoptosis after chronic cocaine abuse [J]. Int J Mol Sci，2014，15（4）：5988-6001.
[10] Krzyzowska M，Baska P，Grochowska A，et al. Fas/FasL pathway participates in resolution of mucosal inflammatory response early during HSV-2 infection [J]. Immunobiology，2014，219（1）：64-77.
[11] Bayram S，Kizilay G，Topcu-Tarladacalisir Y. Evaluation of the Fas/FasL signaling pathway in diabetic rat testis [J]. Biotech Histochem，2016，91（3）：204-211.
[12] Milanovic D，Pesic V，Loncarevic-Vasiljkovic N，et al. The Fas Ligand/Fas Death Receptor Pathways Contribute to Propofol-Induced Apoptosis and Neuroinflammation in the Brain of Neonatal Rats [J]. Neurotox Res，2016，30（3）：434-452.
[13] Zhang Y，Yan H. Effect of simvastatin on retinal Bcl-2/Bax expression and cell apoptosis in rats with ischemia-reperfusion injury [J]. Zhonghua Yan Ke Za Zhi，2014，50（11）：826-832.
[14] Jiang Y，Xu H，Wang J. Alantolactone induces apoptosis of human cervical cancer cells via reactive oxygen species generation，glutathione depletion and inhibition of the Bcl-2/Bax signaling pathway [J]. Oncol Lett，2016，11（6）：4203-4207.
[15] Skala E，Sitarek P，Toma M，et al. Inhibition of human glioma cell proliferation by altered Bax/Bcl-2-p53 expression and apoptosis induction by Rhaponticum carthamoides extracts from transformed and normal roots [J]. J Pharm Pharmacol，2016，68（11）：1454-1464.
[16] Zhu P，Zhao MY，Li XH，et al. Effect of low temperatures on BAX and BCL2 proteins in rats with spinal cord ischemia reperfusion injury [J]. Genet Mol Res，2015，14（3）：10490-10499.
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