目的 探讨补阳还五汤（BYHWD）对TGF-β1诱导的人黄韧带细胞异常增殖与纤维化的影响，并阐明其通过PHLPP1/AKT/mTORC1信号通路发挥作用的分子机制。 方法 体外培养人黄韧带原代细胞，采用TGF-β1诱导构建纤维化细胞模型，以BYHWD含药血清干预；基于CCK-8/EdU进行细胞增殖活性检测，Western blot检测增殖标志物（PCNA、Ki-67）、纤维化标志物（Collagen I、Collagen Ⅲ、α-SMA、Fibronectin）及通路蛋白（PHLPP1、p-AKT、AKT、p-S6K、S6K、p-S6、S6）表达；构建shPHLPP1慢病毒载体进行基因敲减挽救实验，验证通路依赖性。 结果 BYHWD含药血清可显著抑制TGF-β1诱导的黄韧带细胞增殖，下调PCNA、Ki-67表达；降低Collagen I、Collagen Ⅲ、α-SMA、Fibronectin水平，减轻细胞纤维化；同时上调PHLPP1蛋白表达，降低p-AKT/AKT、p-S6K/S6K、p-S6/S6比值，抑制AKT/mTORC1通路异常激活。敲减PHLPP1后，BYHWD对细胞增殖、纤维化的抑制作用，以及对AKT/mTORC1通路的阻断效应均被显著逆转。 结论 BYHWD可通过上调PHLPP1表达、抑制AKT/mTORC1通路异常激活，进而抑制黄韧带细胞异常增殖与纤维化，为其治疗气虚血瘀型黄韧带肥厚、腰椎管狭窄症提供实验依据与分子靶点。

Objective To investigate the effects of Buyang Huanwu Decoction （BYHWD） on the abnormal proliferation and fibrosis of human ligamentum flavum cells （LFCs） induced by transforming growth factor-β1 （TGF-β1）， and to elucidate the underlying molecular mechanisms mediated by the PHLPP1/AKT/mTORC1 signaling pathway. Methods Primary human LFCs were cultured in vitro and stimulated with TGF-β1 to establish a fibrotic cell model， followed by intervention with BYHWD-medicated serum. Cell proliferation was assessed using CCK-8 and EdU assays. Western blotting was performed to detect the protein expression levels of proliferation-related markers （PCNA， Ki-67）， fibrosis-related markers （collagen Ⅰ， collagen Ⅲ， α-SMA， and fibronectin）， and key signaling proteins （PHLPP1， p-AKT， total AKT， p-S6K， total S6K， p-S6， and total S6）. Furthermore， a lentiviral vector carrying shPHLPP1 was constructed to perform PHLPP1 knockdown rescue experiments， thereby verifying the pathway dependence of BYHWD efficacy. Results BYHWD-medicated serum markedly suppressed TGF-β1-induced proliferation of LFCs and downregulated the expression of PCNA and Ki-67. Concurrently， BYHWD reduced the protein levels of collagen I， collagen III， α-SMA， and fibronectin， thereby alleviating cellular fibrosis. Mechanistically， BYHWD upregulated PHLPP1 expression and decreased the ratios of phosphorylated to total proteins （p-AKT/AKT， p-S6K/S6K， and p-S6/S6）， thus blocking the hyperactivation of the AKT/mTORC1 cascade. Notably， PHLPP1 knockdown significantly reversed the inhibitory effects of BYHWD on cell proliferation and fibrosis， as well as its suppressive effect on the AKT/mTORC1 pathway. Conclusions BYHWD attenuates the aberrant proliferation and fibrosis of LFCs by upregulating PHLPP1 and suppressing the hyperactivation of the AKT/mTORC1 signaling pathway. This study provides experimental evidence and identifies potential molecular targets for the clinical application of BYHWD in treating ligamentum flavum hypertrophy and lumbar spinal stenosis associated with Qi deficiency and blood stasis syndrome.