Ro 31-8220对脂多糖诱导的肝毒性及大鼠库普弗细胞肿瘤坏死因子释放的影响。
Effects of Ro 31-8220 on lipopolysaccharides-induced hepatotoxicity and release of tumor necrosis factor from rat Kupffer cells.
作者信息
Lin W, Zhang J P, Hu Z L, Feng Z H, Qian D H
机构信息
Research Laboratory of Natural and Synthetic Drugs, College of Pharmacy, Second Military Medical University, Shanghai, China.
出版信息
Zhongguo Yao Li Xue Bao. 1997 Jan;18(1):85-7.
AIM
To investigate protein kinase C (PKC) functions on lipopolysaccharide (LPS)-induced hepatotoxicity, a new potent PKC inhibitor Ro 31-8220 (Ro) was used to detect its effect on LPS-induced hepatotoxicity in rat hepatocytes and tumor necrosis factor (TNF) release from rat Kupffer cells (KC).
METHODS
Hepatocytes (containing KC) were incubated with LPS (10 mg.L-1) and Ro (0.1-10 mumol.L-1) for 24 h, alanine aminotransferase (AlaA) leakage in the culture as indication of hepatotoxicity. The TNF activity in the supernatant of rat KC culture with LPS in the presence of Ro (0.1-10 mumol.L-1) was monitored by the L929 target cell lytic assay.
RESULTS
Ro (0.1-10 mumol.L-1) reduced AlaA leakage in the hepatocyte culture. Ro inhibited dose-dependently the LPS-induced TNF production from rat KC.
CONCLUSION
PKC inhibitor Ro protects the hepatocytes from LPS-induced cytotoxicity and inhibits the LPS-induced TNF production from rat KC.
目的
为研究蛋白激酶C（PKC）在脂多糖（LPS）诱导的肝毒性中的作用，使用一种新型强效PKC抑制剂Ro 31-8220（Ro）来检测其对大鼠肝细胞中LPS诱导的肝毒性以及大鼠枯否细胞（KC）释放肿瘤坏死因子（TNF）的影响。
方法
将肝细胞（含KC）与LPS（10 mg.L-1）和Ro（0.1 - 10 μmol.L-1）孵育24小时，以培养物中丙氨酸转氨酶（AlaA）泄漏作为肝毒性的指标。通过L929靶细胞裂解试验监测在Ro（0.1 - 10 μmol.L-1）存在下LPS刺激的大鼠KC培养上清液中的TNF活性。
结果
Ro（0.1 - 10 μmol.L-1）减少了肝细胞培养物中的AlaA泄漏。Ro剂量依赖性地抑制LPS诱导的大鼠KC产生TNF。
结论
PKC抑制剂Ro保护肝细胞免受LPS诱导的细胞毒性，并抑制LPS诱导的大鼠KC产生TNF。
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