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首页> 外文期刊>Life sciences >TUMOR NECROSIS FACTOR-ALPHA AND NITRIC OXIDE PRODUCTION IN ENDOTOXIN-PRIMED RATS ADMINISTERED CARBON TETRACHLORIDE
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TUMOR NECROSIS FACTOR-ALPHA AND NITRIC OXIDE PRODUCTION IN ENDOTOXIN-PRIMED RATS ADMINISTERED CARBON TETRACHLORIDE

机译：内毒素开始的大鼠四氯化碳中肿瘤坏死因子-α和一氧化氮的产生

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Tumor necrosis factor-alpha (TNF alpha) is elevated in the sera of rats administered non-lethal doses of carbon tetrachloride (CCl4) followed by endotoxin. Elevated TNF alpha levels are correlated with the increased release of hepatic enzymes indicating hepatic damage. Under these conditions, nitric oxide (NO) was also produced in the liver as evidenced by the formation of nitrosyl complexes which were measured by electron paramagnetic resonance (EPR) spectroscopy. Decreased nitrosyl complex formation occurred in livers following treatment with either an inhibitor of macrophage activation (gadolinium trichloride; GdCl3), an inhibitor of cytokine responses (dexamethasone) or a NO synthase inhibitor (N-G-monomethyl-L-arginine; 1-NMA). GdCl3 or dexamethasone treatment decreased, while 1-NMA treatment increased, TNF alpha serum level. Taken together, these data suggest that TNF alpha and NO are induced following CCl4 and LPS exposure and may be important regulators in the hepatotoxicity of this liver injury model. [References: 30]
机译：在给予非致命剂量的四氯化碳（CCl4）和内毒素后，大鼠血清中的肿瘤坏死因子-α（TNFα）升高。 TNFα水平升高与肝酶释放增加相关，表明肝损伤。在这些条件下，肝脏中还会产生一氧化氮（NO），这可以通过亚电子顺磁共振（EPR）光谱法测定亚硝酰基配合物的形成来证明。用巨噬细胞活化抑制剂（三氯化ga; GdCl3），细胞因子应答抑制剂（地塞米松）或NO合酶抑制剂（N-G-单甲基-L-精氨酸; 1-NMA）治疗后，肝脏中亚硝酰基复合物的形成减少。 GdCl3或地塞米松治疗减少，而1-NMA治疗增加，TNFα血清水平。综上所述，这些数据表明TNFα和NO是在CCl4和LPS暴露后诱导的，并且可能是该肝损伤模型的肝毒性的重要调节剂。 [参考：30]

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