目的 观察牛磺酸（TAU）对环磷酰胺（CTX）致小鼠免疫抑制及肾脏免疫微环境紊乱的保护作用，探讨其调控PI3K/Akt信号通路的分子机制。方法 60 只ICR小鼠随机分为对照组、CTX 组、牛磺酸低剂量(TAU-L, 100 mg/kg）及高剂量组（TAU-H, 400 mg/kg），每组 15 只。对照组每日腹腔注射生理盐水0.2 ml，连续12 d；CTX组前7 d注射生理盐水0.2 ml，第8~12天腹腔注射CTX 0.2 ml（80 mg/kg），连续5 d构建模型；TAU-L、TAU-H组每日腹腔注射对应浓度牛磺酸0.2 ml，连续12 d，同时第8~12天同步注射CTX 0.2 ml（80 mg/kg）。检测小鼠体质量增长率、免疫器官指数、迟发型超敏反应（DTH）强度；血常规及生化检测外周血免疫细胞计数、血清总蛋白（TP）、IgM、白细胞介素（IL）-10及肿瘤坏死因子α（TNF-α）水平；HE 染色观察脾脏及肾脏病理学形态；检测肾脏超氧化物歧化酶（SOD）活性与丙二醛（MDA）含量；Real-time PCR及免疫组织化学检测脾脏、肾脏PI3K/Akt 信号通路相关分子mRNA 与蛋白表达。结果 与对照组相比，CTX 组小鼠免疫器官指数、DTH 强度、外周血免疫细胞数量及血清 IgM、TP 水平显著降低，IL-10水平升高、TNF-α水平降低（P<0.05 或 P<0.0001）；脾脏及肾脏组织形态异常，肾脏 SOD 活性降低、MDA 含量升高（P<0.05）；脾脏及肾脏 PI3K/Akt 信号通路相关分子表达下调（P<0.05 或 P<0.01）。牛磺酸高剂量组上述指标显著改善（P<0.05），低剂量组部分指标有改善但差异无统计学意义（P>0.05）。结论 牛磺酸可激活PI3K/Akt信号通路，改善CTX诱导的小鼠免疫功能低下及肾脏免疫微环境紊乱，增强肾脏抗氧化能力。

Objective To explore the protective effect of taurine（TAU） on cyclophosphamide (CTX)-induced immunosuppression and renal immune microenvironment disorders in mice, and clarify its molecular mechanism regulating the PI3K/Akt signaling pathway. Methods Sixty ICR mice were randomly divided into control group, CTX group, low-dose taurine group (TAU-L, 100 mg/kg) and high-dose taurine group (TAU-H, 400 mg/kg), with 15 mice in each group. The control group was intraperitoneally injected with 0.2 ml normal saline daily for 12 consecutive days. The CTX group was injected with 0.2 ml normal saline for the first 7 days, and then intraperitoneally injected with 0.2 ml CTX (80 mg/kg) from day 8 to day 12 for 5 consecutive days to establish the model. The TAU-L and TAU-H groups were intraperitoneally injected with 0.2 ml taurine at the corresponding concentrations daily for 12 consecutive days, and synchronously injected with 0.2 ml CTX (80 mg/kg) from day 8 to day 12. The body weight growth rate, immune organ indices, and delayed-type hypersensitivity (DTH) intensity were measured. Routine blood test and biochemical detection were used to determine peripheral blood immune cell count, serum total protein (TP), IgM, interleukin (IL)-10 and tumor necrosis factor α (TNF-α) levels. HE staining was used to observe the pathological morphology of spleen and kidney. The activity of superoxide dismutase (SOD) and content of malondialdehyde (MDA) in kidney were detected. Real-time PCR and immunohistochemistry were used to detect the mRNA and protein expressions of PI3K/Akt pathway-related molecules in spleen and kidney. Results Compared with the control group, the CTX group showed significantly decreased immune organ indices, DTH intensity, peripheral blood immune cell count, serum IgM and TP levels, increased IL-10 level and decreased TNF-α level (P<0.05 or P<0.0001); Abnormal pathological morphology of spleen and kidney, decreased renal SOD activity and increased MDA content (P<0.05); Down-regulated expressions of PI3K/Akt pathway-related molecules in spleen and kidney (P<0.05 or P<0.01). The above indicators were significantly improved in the high-dose taurine group (P<0.05), while some indicators in the low-dose taurine group were improved without statistical significance (P>0.05). Conclusion Taurine can activate the PI3K/Akt signaling pathway to improve CTX-induced immunosuppression and renal immune microenvironment disorder, enhance renal antioxidant capacity.