Emergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, People's Republic of China.
Inflammation. 2016 Apr;39(2):575-82. doi: 10.1007/s10753-015-0282-2.
Acute kidney injury (AKI) is a serious complication of sepsis, which has a high mortality rate. Growth arrest-specific protein 6 (Gas6), the protein product of the growth arrest specific gene 6, has been shown to have an anti-apoptotic effect as well as pro-survival capability. Here, we investigated the effects of Gas6 on sepsis-associated AKI in mice subjected to cecal ligation and puncture (CLP). We found that the administration of rmGas6 significantly reduced serum urea nitrogen and creatinine and improved the survival of septic mice. Furthermore, the renal pathological damage induced by CLP was attenuated by rmGas6 treatment. Finally, rmGas6 reduced the renal tissue apoptotic index and the expression of Bax, while it upregulated the expression of Bcl-2. The data suggest that rmGas6 might be used as a potential therapeutic agent for sepsis-induced AKI.
急性肾损伤(AKI)是脓毒症的严重并发症,死亡率很高。生长停滞特异性蛋白 6(Gas6)是生长停滞特异性基因 6 的蛋白产物,已被证明具有抗细胞凋亡作用和促生存能力。在这里,我们研究了 Gas6 对接受盲肠结扎和穿刺(CLP)的脓毒症相关 AKI 小鼠的影响。我们发现,rmGas6 的给药显著降低了血清尿素氮和肌酐,并提高了脓毒症小鼠的存活率。此外,rmGas6 治疗减轻了 CLP 引起的肾脏病理损伤。最后,rmGas6 降低了肾组织的凋亡指数和 Bax 的表达,同时上调了 Bcl-2 的表达。数据表明,rmGas6 可能可作为治疗脓毒症诱导的 AKI 的潜在治疗剂。