Protective effects of estrogen (E2) on traumatic brain injury (TBI) have been determined. In this study, the hepatoprotective effects of E2 after TBI through its receptors and oxidative stress regulation have been evaluated. Diffuse TBI induced by the Marmarou method in male rats. G15, PHTPP, MPP, and ICI182–780 as selective antagonists of E2 were injected before TBI. The results indicated that TBI induces a significant increase in liver enzymes [Alkaline phosphatase (ALP), Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), Glutamyl transferase (GGT)], and oxidants levels [Malondialdehyde (MDA), Nitric oxide (NO)] and decreases in antioxidant biomarkers [Glutathione peroxidase (GPx) and Superoxide dismutase (SOD)] in the brain and liver, and plasma. We also found that E2 significantly preserved levels of these biomarkers and enzymatic activity. All antagonists inhibited the effects of E2 on increasing SOD and GPx. Also, the effects of E2 on brain MDA levels were inhibited by all antagonists, but in the liver, only ICI + G15 + E2 + TBI group was affected. The impacts of E2 on brain and liver and plasma NO levels were inhibited by all antagonists. The current findings demonstrated that E2 probably improved liver injury after TBI by modulating oxidative stress. Also, both classic (ERβ, ERα) and non-classic [G protein-coupled estrogen receptor (GPER)] receptors are affected in the protective effects of E2.

已确定雌激素（E2）对颅脑外伤（TBI）的保护作用。在这项研究中，已评估了E2在TBI后通过其受体和氧化应激调节的保肝作用。Marmarou方法诱导的雄性大鼠弥漫性TBI。在TBI之前注射G15，PHTPP，MPP和ICI182-780作为E2的选择性拮抗剂。结果表明TBI诱导肝酶[碱性磷酸酶（ALP），天冬氨酸氨基转移酶（AST），丙氨酸氨基转移酶（ALT），谷氨酰胺基转移酶（GGT）]和氧化剂水平[丙二醛（MDA），一氧化氮（ NO）]并降低脑，肝脏和血浆中的抗氧化剂生物标志物[谷胱甘肽过氧化物酶（GPx）和超氧化物歧化酶（SOD）]。我们还发现E2可以显着保留这些生物标记物和酶活性的水平。所有拮抗剂均抑制E2对增加SOD和GPx的作用。同样，E2对脑MDA水平的作用也被所有拮抗剂抑制，但在肝脏中，仅ICI + G15 + E2 + TBI组受到影响。E2对脑，肝和血浆NO水平的影响均被所有拮抗剂抑制。目前的发现表明，E2可能通过调节氧化应激改善了TBI后的肝损伤。同样，经典（ERβ，ERα）和非经典[G蛋白偶联雌激素受体（GPER）]受体均会影响E2的保护作用。仅ICI + G15 + E2 + TBI组受到影响。E2对脑，肝和血浆NO水平的影响均被所有拮抗剂抑制。目前的发现表明，E2可能通过调节氧化应激改善了TBI后的肝损伤。同样，经典（ERβ，ERα）和非经典[G蛋白偶联雌激素受体（GPER）]受体均会影响E2的保护作用。仅ICI + G15 + E2 + TBI组受到影响。E2对脑，肝和血浆NO水平的影响均被所有拮抗剂抑制。目前的发现表明，E2可能通过调节氧化应激改善了TBI后的肝损伤。同样，经典（ERβ，ERα）和非经典[G蛋白偶联雌激素受体（GPER）]受体均会影响E2的保护作用。