Taibi-Djennah Zahida, Laraba-Djebari Fatima
USTHB, Faculty of Biological Sciences, Laboratory of Cellular and Molecular Biology, BP 32 El-Alia, Bab Ezzouar, Algiers, Algeria.
USTHB, Faculty of Biological Sciences, Laboratory of Cellular and Molecular Biology, BP 32 El-Alia, Bab Ezzouar, Algiers, Algeria.
Int Immunopharmacol. 2015 Jul;27(1):122-9. doi: 10.1016/j.intimp.2015.05.002. Epub 2015 May 12.
Androctonus australis hector (Aah) venom and its neurotoxins may affect the neuro-endocrine immunological axis due to their binding to ionic channels of axonal membranes. This binding leads to the release of neurotransmitters and immunological mediators accompanied by pathophysiological effects. Although the hyperglycemia induced by scorpion venom is clearly established, the involved mediators in these deregulations are unknown. The strong relationship between inflammation and the wide variety of physiological processes can suggest that the activation of the inflammatory response and the massive release of IL-6 and TNF-α release induced by the venom may induce hyperglycemia and various biological disorders. We therefore investigated in this study the contribution of IL-6 and TNF-α in the modulation of inflammatory response and metabolic disorder induced by Aah venom. Obtained results revealed that Aah venom induced inflammatory response characterized by significant increase of inflammatory cells in sera and tissues homogenates accompanied by hyperglycemia and hyperinsulinemia, suggesting that the venom induced insulin resistance. It also induced severe alterations in hepatic parenchyma associated to metabolic disorders and imbalanced redox status. Cytokine antagonists injected 30 min prior to Aah venom allowed a significant reduction of inflammatory biomarker and plasma glucose levels, they also prevented metabolic disorders, oxidative stress and hepatic tissue damage induced by Aah venom. In conclusion, IL-6 and TNF-α appear to play a crucial role in the inflammatory response, hyperglycemia and associated complications to glucose metabolism disorders (carbohydrate and fat metabolism disorders, oxidative stress and hepatic damage) observed following scorpion envenoming.
澳毒蛛（Androctonus australis hector，Aah）毒液及其神经毒素可能因其与轴突膜离子通道的结合而影响神经 - 内分泌免疫轴。这种结合导致神经递质和免疫介质的释放，并伴有病理生理效应。尽管蝎毒诱导的高血糖已明确证实，但这些调节异常中涉及的介质尚不清楚。炎症与多种生理过程之间的紧密关系表明，毒液诱导的炎症反应激活以及IL - 6和TNF - α的大量释放可能会诱导高血糖和各种生物学紊乱。因此，我们在本研究中调查了IL - 6和TNF - α在Aah毒液诱导的炎症反应和代谢紊乱调节中的作用。获得的结果显示，Aah毒液诱导了炎症反应，其特征是血清和组织匀浆中的炎症细胞显著增加，同时伴有高血糖和高胰岛素血症，这表明毒液诱导了胰岛素抵抗。它还导致肝实质的严重改变，与代谢紊乱和氧化还原状态失衡有关。在注射Aah毒液前30分钟注射细胞因子拮抗剂可显著降低炎症生物标志物和血糖水平，还可预防Aah毒液诱导的代谢紊乱、氧化应激和肝组织损伤。总之，IL - 6和TNF - α似乎在蝎毒中毒后观察到的炎症反应、高血糖以及与糖代谢紊乱相关的并发症（碳水化合物和脂肪代谢紊乱、氧化应激和肝损伤）中起关键作用。
