Lin Miao, Li Long, Li Liping, Pokhrel Gaurab, Qi Guisheng, Rong Ruiming, Zhu Tongyu
Department of Urology, Fudan University Zhongshan Hospital, Shanghai, China.
BMC Complement Altern Med. 2014 Jan 13;14:19. doi: 10.1186/1472-6882-14-19.
Renal ischemia-reperfusion injury (IRI) increases the rates of acute kidney failure, delayed graft function, and early mortality after kidney transplantation. The pathophysiology involved includes oxidative stress, mitochondrial dysfunction, and immune-mediated injury. The anti-oxidation, anti-apoptosis, and anti-inflammation properties of baicalin, a flavonoid glycoside isolated from Scutellaria baicalensis, have been verified. This study therefore assessed the effects of baicalin against renal IRI in rats.
Baicalin was intraperitoneally injected 30 min before renal ischemia. Serum and kidneys were harvested 24 h after reperfusion. Renal function and histological changes were assessed. Markers of oxidative stress, the Toll-like receptor (TLR)2 and TLR4 signaling pathway, mitochondrial stress, and cell apoptosis were also evaluated.
Baicalin treatment decreased oxidative stress and histological injury, and improved kidney function, as well as inhibiting proinflammatory responses and tubular apoptosis. Baicalin pretreatment also reduced the expression of TLR2, TLR4, MyD88, p-NF-κB, and p-IκB proteins, as well as decreasing caspase-3 activity and increasing the Bcl-2/Bax ratio.
Baicalin may attenuate renal ischemia-reperfusion injury by inhibiting proinflammatory responses and mitochondria-mediated apoptosis. These effects are associated with the TLR2/4 signaling pathway and mitochondrial stress.
肾缺血再灌注损伤(IRI)会增加肾移植后急性肾衰竭、移植肾功能延迟恢复及早期死亡率。其涉及的病理生理过程包括氧化应激、线粒体功能障碍及免疫介导损伤。黄芩苷是从黄芩中分离出的一种黄酮苷,其抗氧化、抗凋亡及抗炎特性已得到证实。因此,本研究评估了黄芩苷对大鼠肾IRI的影响。
在肾缺血前30分钟腹腔注射黄芩苷。再灌注24小时后采集血清和肾脏。评估肾功能和组织学变化。还评估了氧化应激标志物、Toll样受体(TLR)2和TLR4信号通路、线粒体应激及细胞凋亡情况。
黄芩苷治疗可降低氧化应激和组织学损伤,改善肾功能,同时抑制促炎反应和肾小管凋亡。黄芩苷预处理还可降低TLR2、TLR4、MyD88、p-NF-κB和p-IκB蛋白的表达,降低半胱天冬酶-3活性并提高Bcl-2/Bax比值。
黄芩苷可能通过抑制促炎反应和线粒体介导的凋亡减轻肾缺血再灌注损伤。这些作用与TLR2/4信号通路及线粒体应激有关。