Effects of on Low T3 syndrome astrocyte homeostasis in patients with bisphenol A-associated intracerebral hemorrhage

Author:

Wang GuopingORCID,Chen Jinhua,Qiao Zhongdong,Guo Dongxing,Guo Ping,Wang Aiven,Sun Wanli,Lyu Jiyuan

Abstract

AbstractBackground and PurposeWe aimed to assess sex differences in lipid metabolism disorders in patients with BPA-related intracerebral hemorrhage, as well as changes in β3-adrenoceptors and oxidative stress parameters, and to explore potential mechanisms of intestinal flora on the functional homeostasis of cerebral astrocytes.MethodsHere, a multicenter longitudinal retrospective study was conducted in 200 patients with intracerebral hemorrhage compared with normal controls. Serum thyroid function, blood lipids and subclasses, superoxide dismutase and malondialdehyde were detected. Active oxygen species and reactive oxidative products in brain tissue were detected by fluorescein labeling apparatus. Lipid metabolism and oxidative stress regulate messenger proteins, as well as changes in intestinal flora and astrocyte expression.ResultsSerum lipoprotein β levels of LT3 male patients were significantly increased, with gender differences compared with female patients. β3-adrenergic receptor and Neuregulin –1 expression changes, targeted regulation of fat and reduce oxidative stress response. The increased expression of messenger protein prompts activation of brain astrocytes. The intestinal flora study found that the alpha diversity index in the low T3 group was higher than that in the control group, and Spearman correlation analysis showed that low T3 level was negatively correlated with lipid metabolism disorders and oxidative stress.ConclusionsBisphenol A and oxidative stress were significantly related to the high risk of cerebral hemorrhage. The changes of inflammatory cytokines and the ratio expression of connexin 43/Yes associated proteins in the gut brain axis drive activated astrocytes and microglia to jointly maintain the homeostasis of cerebral vascular microenvironment.Trial registrationThe trial is registered at clinical.gov (www.medresman.ChiCTR1900023626)

Publisher

Cold Spring Harbor Laboratory

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