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首页> 外文期刊>Journal of applied toxicology >Inhibitory effect of MIL glycoprotein on expression of pro-inflammatory mediators in carbon tetrachloride-induced mice liver damage.
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Inhibitory effect of MIL glycoprotein on expression of pro-inflammatory mediators in carbon tetrachloride-induced mice liver damage.

机译:MIL糖蛋白对四氯化碳诱导的小鼠肝损伤中促炎性介质表达的抑制作用。

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The aim of the present study was to evaluate immunomodulatory and hepatoprotective effects of glycoprotein isolated from Morus indica Linne (MIL glycoprotein) on carbon tetrachloride (CCl(4) )-induced liver injury. In the present study, MIL glycoprotein (5 and 10 mg kg(-1) body weight) was administered to ICR mice for 7 days prior to CCl(4) treatment. We evaluated the activities of alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and thiobarbituric acid-reactive substances (TBARS), and expression of inflammation-related mediators including cyclooxygenase (COX)-2, tumor necrosis factor (TNF)-alpha, and interleukin (IL)-1 beta in CCl(4) -treated mice. Our results revealed that MIL glycoprotein reduced the activities of ALT, LDH and TBARS in serum from CCl(4) -treated mice. We also found that MIL glycoprotein reduced the activity of COX-2 and expression of TNF-alpha and IL-1 beta in liver from CCl(4) -treated mice. Moreover, administration of MIL glycoprotein suppressed on stress-activated protein kinase/c-jun N-terminal kinase phosphorylation and activator protein-1 transcriptional activation in livers from CCl(4) -treated mice. The results from these experiments indicate that MIL glycoprotein effectively protects against liver injury, mainly through downregulation of oxidative stress and the inflammatory response. In conclusion, we suggest that the MIL glycoprotein might be one component of health supplements for prevention of liver diseases.
机译:本研究的目的是评估从Mor桑分离的糖蛋白(MIL糖蛋白)对四氯化碳(CCl(4))诱导的肝损伤的免疫调节和肝保护作用。在本研究中,在CCl(4)治疗之前,对ICR小鼠给予MIL糖蛋白(5和10 mg kg(-1)体重)给予7天。我们评估了丙氨酸转氨酶(ALT),乳酸脱氢酶(LDH)和硫代巴比妥酸反应性物质(TBARS)的活性,以及​​炎症相关介质的表达,包括环氧合酶(COX)-2,肿瘤坏死因子(TNF)-alpha ,以及CCl(4)处理的小鼠中的白介素(IL)-1 beta。我们的结果表明,MIL糖蛋白可降低CCl(4)处理小鼠血清中ALT,LDH和TBARS的活性。我们还发现,MIL糖蛋白降低了CCl(4)处理的小鼠肝脏中COX-2的活性以及TNF-α和IL-1β的表达。此外,MIL糖蛋白的管理抑制了来自CCl(4)处理的小鼠肝脏中的应力激活蛋白激酶/ c-jun N末端激酶磷酸化和激活蛋白1转录激活。这些实验的结果表明,MIL糖蛋白主要通过下调氧化应激和炎症反应有效地保护肝脏免受肝损伤。总之,我们建议MIL糖蛋白可能是预防肝病的健康补品之一。

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