目的 研究加味通脉化癥汤干预Wnt/β-连环蛋白（β-catenin）通路对子宫腺肌病（AM）小鼠病灶细胞凋亡的影响，探讨其作用机制。 方法 采用他莫昔芬造模法建立AM小鼠模型。将造模成功的21只小鼠按随机数字表法分为模型组、加味通脉化癥汤组、孕三烯酮组各7只，另设7只雌性小鼠为空白组。加味通脉化癥汤组灌胃加味通脉化癥汤36.51 g/kg，1次/d；孕三烯酮组灌胃孕三烯酮0.32 mg/kg，2次/周；空白组和模型组灌胃等体积的生理盐水，1次/d。干预2个月后，采用HE染色观察子宫组织形态，采用ELISA法检测血清糖类蛋白125（CA125）、泌乳素（PRL）水平，采用PCR检测子宫组织Wnt3a、β-catenin mRNA水平，采用Western blot法检测子宫组织Wnt3a、β-catenin、Bax、Bcl-2蛋白表达。 结果 与模型组比较，加味通脉化癥汤组小鼠血清CA125、PRL水平降低（P<0.05），子宫组织Wnt3a、β-catenin mRNA水平降低（P<0.05），Wnt3a、β-catenin、Bcl-2蛋白表达降低（P<0.05），Bax蛋白表达升高（P<0.05）。 结论 加味通脉化癥汤通过降低AM模型小鼠中血清CA125和PRL水平，缓解病灶进展，并可下调Bcl-2表达和上调Bax表达，促进小鼠异位病灶细胞凋亡，其作用机制可能与抑制Wnt/β-catenin通路相关蛋白表达有关。 Objective To study the effects of intervention of Jiawei Tongmai Huazhi Decoction in the Wnt/β-catenin pathway on apoptosis of lesion cells in mice with adenomyosis (AM) To discuss its mechanism of action. Methods The AM mouse model was established using tamoxifen. The mice were divided into model group, Jiawei Tongmai Huazhi Decoction group, and progesterone group according to random number table method, with 7 mice in each group. Additionally, a blank group of 7 female mice was set up. Jiawei Tongmai Huazhi Decoction group received oral administration of Jiawei Tongmai Huazhi Decoction at a dosage of 36.51 g/kg/day, once daily. The progesterone group received oral administration of progesterone at a dose of 0.32 mg/kg twice a week. The blank group and model group received oral administration of the same volume of physiological saline once daily. After 2 months of intervention, the morphology of uterine tissues was observed by HE staining. The levels of carbohydrate antigen 125 (CA125) and prolactin (PRL) in the serum were measured by ELISA. The mRNA levels of Wnt3a and β-catenin in uterine tissues were determined by PCR. The protein expressions of Wnt3a, β-catenin, Bax, and Bcl-2 in uterine tissues were detected by Western blot. Results Compared with the model group, the levels of serum CA125 and PRL were reduced in the Jiawei Tongmai Huazhi Decoction group (P<0.05). The protein expressions of Wnt3a, β-catenin, and Bcl-2 were also reduced (P<0.05), the protein expressions of Wnt3a, β-catenin, and Bcl-2 decreased (P<0.05), while the protein expressions of Bax increased (P<0.05). Conclusion Jiawei Tongmai Huazhi Decoction alleviates the progression of lesions by reducing serum CA125 and PRL levels in AM model mice, and can down-regulate Bcl-2 expression and up-regulate Bax expression, promoting apoptosis of ectopic lesion cells in mice. Its mechanism of action may be related to the inhibition of Wnt/β-catenin pathway related expression proteins.
Mechanism study on the intervention of Jiawei Tongmai Huazheng Decoction on Wnt/β-catenin pathway promoting apoptosis of lesion cells in mice model of adenomyosis
Objective To study the effects of intervention of Jiawei Tongmai Huazhi Decoction in the Wnt/β-catenin pathway on apoptosis of lesion cells in mice with adenomyosis (AM) To discuss its mechanism of action. Methods The AM mouse model was established using tamoxifen. The mice were divided into model group, Jiawei Tongmai Huazhi Decoction group, and progesterone group according to random number table method, with 7 mice in each group. Additionally, a blank group of 7 female mice was set up. Jiawei Tongmai Huazhi Decoction group received oral administration of Jiawei Tongmai Huazhi Decoction at a dosage of 36.51 g/kg/day, once daily. The progesterone group received oral administration of progesterone at a dose of 0.32 mg/kg twice a week. The blank group and model group received oral administration of the same volume of physiological saline once daily. After 2 months of intervention, the morphology of uterine tissues was observed by HE staining. The levels of carbohydrate antigen 125 (CA125) and prolactin (PRL) in the serum were measured by ELISA. The mRNA levels of Wnt3a and β-catenin in uterine tissues were determined by PCR. The protein expressions of Wnt3a, β-catenin, Bax, and Bcl-2 in uterine tissues were detected by Western blot. Results Compared with the model group, the levels of serum CA125 and PRL were reduced in the Jiawei Tongmai Huazhi Decoction group (P<0.05). The protein expressions of Wnt3a, β-catenin, and Bcl-2 were also reduced (P<0.05), the protein expressions of Wnt3a, β-catenin, and Bcl-2 decreased (P<0.05), while the protein expressions of Bax increased (P<0.05). Conclusion Jiawei Tongmai Huazhi Decoction alleviates the progression of lesions by reducing serum CA125 and PRL levels in AM model mice, and can down-regulate Bcl-2 expression and up-regulate Bax expression, promoting apoptosis of ectopic lesion cells in mice. Its mechanism of action may be related to the inhibition of Wnt/β-catenin pathway related expression proteins.
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