Guo Zhu-Ying, Wang Shi-Ting, Xu Mang-Hua, Jiao Qiang, Gao Feng-Hou
No. 3 People's Hospital AfFiliated to School of Medicine, Shanghai Jiaotong University, Shanghai 201900, China.
Yao Xue Xue Bao. 2009 Jun;44(6):586-90.
To investigate the protective effects of recombinant human tumor necrosis factor receptor II: IgG Fc fusion protein (rhu TNFR: Fc) against the lipopolysaccharide (LPS) induced intestinal damage of rats and its underlying mechanism. SD rats were randomly divided into four groups: control group, rhuTNFR: Fc group, LPS group and rhu TNFR: Fc + LPS group. Mean arterial pressure (MAP) was continuously monitored and the mortality rates were assessed. The levels of TNF-alpha and its bioactivity in the serum were assessed by ELISA and flow cytometry respectively. Pathologic changes of intestinal tissue were observed by HE staining. The rats of control and rhu TNFR: Fc group all survived with stable MAP, and the low level and bioactivity of TNF-alpha in the serum were maintained. While 83% of the rats in LPS group died by 6 h with the levels and bioactivity of TNF-alpha increasing significantly. In rhu TNFR: Fc + LPS group, the mortality rate of rats dropped to 33%. The TNF-alpha level increased compared with control group but its bioactivity decreased significantly compared with LPS group. The MPO activity and content of MDA decreased significantly. The status of pathological manifestation in the intestine was also ameliorated. These data suggest that rhu TNFR: Fc could protect rats from the acute intestine injury induced by LPS through ablating the rise in serum TNF-alpha level and bioactivity as well as anti-oxidation.
探讨重组人肿瘤坏死因子受体II：IgG Fc融合蛋白（rhu TNFR：Fc）对脂多糖（LPS）诱导的大鼠肠道损伤的保护作用及其潜在机制。将SD大鼠随机分为四组：对照组、rhuTNFR：Fc组、LPS组和rhu TNFR：Fc + LPS组。持续监测平均动脉压（MAP）并评估死亡率。分别采用ELISA和流式细胞术评估血清中TNF-α水平及其生物活性。通过HE染色观察肠道组织的病理变化。对照组和rhu TNFR：Fc组大鼠均存活，MAP稳定，血清中TNF-α水平及生物活性维持在较低水平。而LPS组83%的大鼠在6小时内死亡，TNF-α水平及生物活性显著升高。在rhu TNFR：Fc + LPS组，大鼠死亡率降至33%。TNF-α水平较对照组升高，但生物活性较LPS组显著降低。MPO活性和MDA含量显著降低。肠道病理表现状况也得到改善。这些数据表明，rhu TNFR：Fc可通过消除血清TNF-α水平及生物活性的升高以及抗氧化作用，保护大鼠免受LPS诱导的急性肠道损伤。
