Health Examination Center, Sixth People's Hospital Affiliated to Shanghai Jiao Tong University, Shanghai 200233, China.
Evid Based Complement Alternat Med. 2013;2013:284025. doi: 10.1155/2013/284025. Epub 2013 Jun 19.
This study investigated the anti-inflammatory effects of astragaloside IV(AS-IV) on ischemia/reperfusion (IR) induced acute kidney injury (AKI) in rats. Experimental model of ischemic AKI was induced in rats by bilateral renal artery clamp for 45 min followed by reperfusion of 12 h and 24 h, respectively. AS-IV was orally administered once a day to rats at 10 and 20 mg·kg(-1)·d(-1) for 7 days prior to ischemia. AS-IV pretreatment significantly decreased serum urea, creatinine, and cystatin C levels at 12 h and 24 h of reperfusion in AKI rats. AS-IV pretreatment also ameliorated tubular damage and suppressed the phosphorylation of p65 subunit of NF- κ B in AKI rats. Moreover, NF- κ B and MPO activity as well as serum and tissue levels of TNF- α , MCP-1, and ICAM-1 were elevated in AKI rats. All of these abnormalities were prevented by AS-IV. Furthermore, AS-IV downregulated the mRNA expression of NF- κ B, TNF- α , MCP-1, and ICAM-1 in AKI rats. These results suggest that AS-IV might be developed as a novel therapeutic approach to prevent ischemic AKI through inhibition of NF- κ B mediated inflammatory genes expression.
本研究探讨了黄芪甲苷（AS-IV）对大鼠缺血再灌注（IR）诱导的急性肾损伤（AKI）的抗炎作用。通过双侧肾动脉夹闭 45min 后再灌注 12h 和 24h，分别在大鼠中诱导缺血性 AKI 实验模型。在缺血前 7 天，AS-IV 每天以 10 和 20mg·kg（-1）·d（-1）的剂量口服给予大鼠。AS-IV 预处理可显著降低 AKI 大鼠再灌注 12h 和 24h 时的血清尿素、肌酐和胱抑素 C 水平。AS-IV 预处理还可改善肾小管损伤，并抑制 AKI 大鼠 NF-κB p65 亚基的磷酸化。此外，NF-κB 和 MPO 活性以及血清和组织中 TNF-α、MCP-1 和 ICAM-1 的水平在 AKI 大鼠中升高。所有这些异常均被 AS-IV 所预防。此外，AS-IV 下调了 AKI 大鼠中 NF-κB、TNF-α、MCP-1 和 ICAM-1 的 mRNA 表达。这些结果表明，AS-IV 可能通过抑制 NF-κB 介导的炎症基因表达，成为预防缺血性 AKI 的一种新的治疗方法。
