Xi Chen, Tiange Q U, Hui Jia, Xingwu Duan, Jianhong L I, Kaihui Zhang, Runtian Zhang, Ruijie Wang
Department of Dermatology, Dongzhimen Hospital Beijing University of Chinese Medicine, Beijing 100107, China.
Department of Surgery, Shunyi Hospital, Beijing Hospital of Traditional Chinese Medicine, Beijing 101300, China.
J Tradit Chin Med. 2025 Apr;45(2):303-310. doi: 10.19852/j.cnki.jtcm.2025.02.005.
To explore the mechanisms by which Huoxue Chubi decoction (, HXCB) affects the protein kinase B (Akt)-mammalian target of rapamycin (mTOR) autophagy pathway in scleroderma Balb/c model mice.
A scleroderma model was established in male Balb/c mice, followed by daily administration of HXCB (4.6, 2.3 and 1.15 g·kg·d) for 4 weeks. Bodyweight, epidermal and dermal thickness, dermal collagen levels, cutaneous reactive oxygen species (ROS) levels, Akt, Phosphorylated Akt (p-Akt), mTOR, Phosphorylated mTOR (p-mTOR), B-celllymphoma-2-interacting myosin-like coiled-coil protein 1 (Beclin-1) and microtubule-associated protein A/B-light chain 3 (LC3) protein and messenger ribonucleic acid (mRNA) expression were assessed.
HXCB treatment significantly reduced epidermal and dermal thickness, dermal collagen levels, ROS levels and the mRNA and protein expression of factors in the Akt-mTOR signaling pathway compared to the scleroderma model group. Conversely, mice body weight and autophagy factors Beclin-1 and LC3 were significantly increased in mice receiving HXCB treatment. Moreover, finally, ROS expression positively correlated with skin thickness, collagen contents and the mRNA expression levels of Akt, while the protein and mRNA expression levels of Akt-mTOR pathway-related factors were inversely correlated with the protein and mRNA expression of Beclin-1 and LC3.
HXCB can regulate autophagy by invigorating and promoting blood circulation, thereby reducing blood stasis, facilitating new tissue generation, and contributing to scleroderma treatment. This effect may be attributed to the promotion of autophagy and enhancement of collagen degradation through the reduction of tissue oxidative stress elicited by HXCB.
探讨活血除痹汤（HXCB）对硬皮病Balb/c模型小鼠蛋白激酶B（Akt）-雷帕霉素哺乳动物靶蛋白（mTOR）自噬通路的影响机制。
在雄性Balb/c小鼠中建立硬皮病模型，随后每日给予HXCB（4.6、2.3和1.15 g·kg·d），持续4周。评估体重、表皮和真皮厚度、真皮胶原水平、皮肤活性氧（ROS）水平、Akt、磷酸化Akt（p-Akt）、mTOR、磷酸化mTOR（p-mTOR）、B细胞淋巴瘤-2相互作用的肌球蛋白样卷曲螺旋蛋白1（Beclin-1）和微管相关蛋白A/B轻链3（LC3）蛋白及信使核糖核酸（mRNA）表达。
与硬皮病模型组相比，HXCB治疗显著降低了表皮和真皮厚度、真皮胶原水平、ROS水平以及Akt-mTOR信号通路中各因子的mRNA和蛋白表达。相反，接受HXCB治疗的小鼠体重以及自噬因子Beclin-1和LC3显著增加。此外，最后，ROS表达与皮肤厚度、胶原含量以及Akt的mRNA表达水平呈正相关，而Akt-mTOR通路相关因子的蛋白和mRNA表达水平与Beclin-1和LC3的蛋白和mRNA表达呈负相关。
HXCB可通过活血化瘀来调节自噬，从而减少血瘀，促进新组织生成，有助于硬皮病的治疗。这种作用可能归因于HXCB通过减轻组织氧化应激促进自噬并增强胶原降解。
