目的 探讨雌激素信号对小鼠急性损伤骨骼肌内T细胞浸润与功能极化的影响。  方法 取C57BL/6雄性小鼠100只，雌性小鼠180只。心肌毒素（CTX）诱导小鼠急性胫骨前肌（TA）损伤，对25只雌鼠进行卵巢切除（OVX），10只雄鼠进行假手术（sham）操作。17β-雌二醇（E2）或4-羟基他莫昔芬（4-OHT）皮下注射。将雄、雌鼠各70只分为PBS-雄性、CTX-雄性、PBS-雌性、CTX-雌性组，ELISA检测血清E2水平，HE鉴定肌损伤模型。取雄、雌鼠各20只，免疫荧光（IF）和Real-time PCR检测损伤骨骼肌内雌激素受体（ER）表达。将雄鼠10只、雌鼠40只分为CTX、CTX+E2、CTX+4-OHT、CTX+OVX、CTX+sham组，HE和IF检测损伤肌内炎性浸润。将雌鼠50只分为CTX、CTX+OVX组，IF、流式细胞术检测损伤肌内T细胞的表型或肌纤维再生。    结果 雌鼠血清E2水平、再生肌纤维ERβ蛋白表达显著高于雄鼠。较之对照小鼠，E2处理显著缓解小鼠损伤骨骼肌内炎症程度，4-OHT或OVX处理则反之。OVX小鼠损伤骨骼肌内CD4+ T细胞、辅助性T细胞1（Th1）比例上调，但调节性细胞（Tregs）比例及肌纤维再生显著下调。    结论 雌激素信号是骨骼肌损伤炎症的关键调控因素，体内雌激素缺乏可抑制Tregs功能，从而诱导小鼠损伤肌内Th1反应，加剧肌内炎症、延迟肌修复。 

Objective To investigate the effects of estrogen signaling on T-cell recruitment and polarization in acutely injured skeletal muscle.    Methods One hundred C57BL/6 male mice, one hundred and eighty C57BL/6 female mice were selected. Twenty-five female mice were ovariectomized (OVX) and 10 male mice were taken as the sham-operated (sham). Then, cardiotoxin(CTX) induced tibialis anterior(TA) injury for preparing mice myoinjury model. Subcutaneous injection of 17β-estradiol (E2) or estrogen receptor antagonist 4-hydroxytamoxifen (4-OHT) was performed. A total of 140 mice (70 males and 70 females) were divided into four group including: PBS-male, CTX-male, PBS-female, and CTX-female. Serum estradiol (E2) levels were measured by ELISA, and muscle injury models were validated via HE staining. Subsequently, 20 male and 20 female mice were selected for immunofluorescence (IF) and Real-time PCR to assess estrogen receptors (ER) expression in injured muscle tissue. Further, 10 male and 40 female mice were allocated into five experimental groups, including CTX, CTX+E2, CTX+4-OHT, CTX+OVX, CTX+sham. HE staining and IF were performed to evaluate inflammatory infiltration in the injured muscle. Additionally, 50 female mice were divided into CTX and CTX+OVX groups, and IF combined with flow cytometry were used to analyze T-cell phenotypes and muscle fiber regeneration in the injured muscle.    Results  In vivo, serum E2 and myofiber ERβ increased post-injury in mice of both sexes, significantly higher in females. Compared to the control group, E2 alleviated inflammation, OVX exacerbated inflammation, increased CD4^＋ T-cell infiltration, elevated T helper 1 cell(Th1) response, decreased regulatory T cells(Tregs), impaired regeneration. In vitro, IFN-γ/LPS significantly upregulated ERβ in myotubes.    Conclusion  Estrogen signaling critically regulates muscle inflammation. Estrogen deficiency (OVX) delays repair of skeletal muscle by promoting Th1 response and suppressing Tregs function.