癸酸二(2-乙基己基)酯（DEHP）具有潜在的生殖毒性。补肾天经方案（BSTJFs）对女性生殖能力有益。然而，BSTJF2的细胞毒性比BSTJF1低得多。为了研究BSTJFs对暴露于DEHP的卵巢颗粒细胞的影响，并确定潜在的分子机制，将人卵巢颗粒细胞瘤细胞系（KGN）细胞分为对照组、DEHP组、BSTJF1组和BSTJF2组。DEHP组细胞给予1μM DEHP处理24小时。然后给予200μg/mL BSTJF1或100μg/mL BSTJF2处理24小时。对照组用相同浓度的DMSO（0.1%）处理。测量氧化应激和线粒体功能。测定HDAC3和HSP90AA的mRNA和蛋白质表达水平。同时进行BSTJF2的整合网络药理学分析。DEHP（1μM）显著抑制KGN细胞的增殖率，下降17%；显著提高ROS水平，增长28%；显著提高MDA水平，升高47%；显著降低MMP水平，下降22%；显著降低mtDNA拷贝数，低于30%。DEHP显著增加HDAC3蛋白表达水平21%，增加HSP90AA蛋白表达水平64%。所有这些变化均在BSTJFs作用下显著逆转。整合网络药理学分析揭示HSP90AA是一个关键靶点（度 = 8）。RGFP966和BSTJF2均显著逆转DEHP诱导的HDAC3和HSP90AA表达升高、氧化应激和线粒体损伤的变化。BSTJFs可能通过HDAC3/HSP90AA通路在氧化应激和线粒体损伤方面具有治疗潜力，鼓励进行进一步的临床试验。

di-(2-Ethylhexyl) phthalate (DEHP) has potential reproductive toxicity. Bu-Shen-Tian-Jing formulations (BSTJFs) are beneficial for female reproductive capacity. However, BSTJF2 has much lower cytotoxicity than BSTJF1.To investigate the effects of BSTJFs on ovarian granulosa cells exposed to DEHP and determine the potential molecular mechanisms.Human granulosa-like tumor cell line (KGN) cells were divided into control, DEHP, BSTJF1 and BSTJF2 groups. The DEHP group were given 1 μM DEHP for 24 h. They were then given BSTJF1 at 200 μg/mL or BSTJF2 at 100 μg/mL for 24 h. The control group was treated with the same concentration of DMSO (0.1%). Oxidative stress and mitochondrial function were measured. The mRNA and protein expression levels of HDAC3 and HSP90AA were determined. Integrative network pharmacology analysis of BSTJF2 was also performed.DEHP (1 μM) significantly suppressed the proliferation of KGN cells by 17%, significantly increased ROS levels by 28% and MDA levels by 47%, significantly decreased MMP levels by 22% and mtDNA copy by 30%. DEHP significantly increased protein expression of HDAC3 by 21%and HSP90AA by 64%. All these changes were significantly reversed by BSTJFs. Integrative network pharmacology analysis revealed HSP90AA was a key target (degree = 8). Both RGFP966 and BSTJF2 significantly reversed the increased expression of HDAC3 and HSP90AA, attenuated oxidative stress, and mitochondrial damage which were induced by DEHP.BSTJFs might have therapeutic potential on oxidative stress and mitochondrial damage through the HDAC3/HSP90AA pathway which encourages further clinical trials.