Radioprotective effects of Resveratrol is well known in normal cells exposed to the damaging effects of ionizing radiation however, its potential radioprotective effect on ovarian follicle formation and development is still uncertain. Astonishingly, it has been reported that PARP contributed to the pathogenesis of immune-mediated ovarian injury. In this paper, Resveratrol was tested for its inflammatory, anti-cervical carcinoma activity, and checked its targets poly (ADP-ribose) polymerase 1 (PARP-1) induced premature ovarian failure with a potent enzymatic modulatory activity. Through high-throughput virtual screening method, Resveratrol was screened to find its target. That the compound strongly inhibited cervical carcinoma HT-3 cell. The cell proliferation was evaluated by an CCK-8 assay, and the cell apoptosis was assessed by a flow cytometry. Rat model of premature ovarian failure was used to introduce resveratrol preparation and rtPCR was done to measure expression of apoptosis related markers. We report resveratrol as a potential target for PARP-1 and its modulator from a high-throughput virtual screening method. Resveratrol was measured its anti-cervical carcinoma activity by using an CCK-8 assay, which suggested that the compound strongly inhibited HT-3 cell proliferation, the IC₅₀ value is 0.65 μM. In addition, the compound induced HT-3 cell apoptosis in a dose-response manner. Resveratrol preserves the entire ovarian follicle pool manifested by increasing serum anti-Müllerian hormone (AMH) levels. Study suggest that resveratrol restored ovarian function through increasing AMH levels, and diminishing ovarian inflammation, predominantly modulation of PPAR-1 and inhibition of inflammatory cytokines. Resveratrol was identified targets for PARP-1 from a high-throughput virtual screening method, strongly inhibited PARP-1 protein and HT-3 cell proliferation. Resveratrol is a promising PARP-1 modulator with anti-cervical carcinoma activity, which deserves further investigation.

白藜芦醇的辐射防护作用在暴露于电离辐射破坏作用的正常细胞中是众所周知的，然而，其对卵巢卵泡形成和发育的潜在辐射防护作用仍不确定。令人惊讶的是，据报道，PARP 有助于免疫介导的卵巢损伤的发病机制。在本文中，对白藜芦醇的炎症、抗宫颈癌活性进行了测试，并检查了其靶点聚（ADP-核糖）聚合酶 1 (PARP-1) 诱导的卵巢早衰，具有强大的酶调节活性。通过高通量虚拟筛选方法，筛选出白藜芦醇以找到其靶点。表明该化合物对宫颈癌HT-3细胞有很强的抑制作用。通过CCK-8测定评估细胞增殖，并通过流式细胞术评估细胞凋亡。用大鼠卵巢早衰模型导入白藜芦醇制剂，通过rtPCR检测细胞凋亡相关标志物的表达。我们通过高通量虚拟筛选方法报告白藜芦醇作为 PARP-1 及其调节剂的潜在目标。白藜芦醇通过 CCK-8 试验测定其抗宫颈癌活性，表明该化合物强烈抑制 HT-3 细胞增殖，IC₅₀值为 0.65 μM。此外，该化合物以剂量反应方式诱导 HT-3 细胞凋亡。白藜芦醇通过增加血清抗苗勒管激素 (AMH) 水平来保护整个卵巢卵泡池。研究表明，白藜芦醇通过增加 AMH 水平和减少卵巢炎症，主要是调节 PPAR-1 和抑制炎症细胞因子来恢复卵巢功能。从高通量虚拟筛选方法中，白藜芦醇被确定为 PARP-1 的靶标，强烈抑制 PARP-1 蛋白和 HT-3 细胞增殖。白藜芦醇是一种很有前景的 PARP-1 调节剂，具有抗宫颈癌活性，值得进一步研究。