Yuan Ben, Luo Shuhong, Feng Liulian, Wang Junling, Mao Junbiao, Luo Bingbing
Department of Reproductive Medicine, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Edong Healthcare Group, Huangshi, 435000, Hubei, China.
J Bioenerg Biomembr. 2022 Aug;54(4):191-201. doi: 10.1007/s10863-022-09942-7. Epub 2022 Jul 14.
Polycystic ovary syndrome (PCOS) is featured as a common endocrine disorder in reproductive-aged women, while its pathophysiology is not fully illustrated. This study examined potential actions of resveratrol in PCOS cellular model and explored the underlying interaction between resveratrol and toll-like receptor 2 (TLR2). This study performed the bioinformatics analysis on two microarray datasets (GSE34526 and GSE138518). We found that TLR2 was one of potential hub genes that may be associated with PCOS. Further examination showed that TLR2 was highly expressed in granulosa cells from PCOS group compared with control. The in vitro studies showed that LPS intervention caused an increased expression of TLR2 and the pro-inflammatory mediators, and induced oxidative stress in the granulosa cells, which was concentration-dependently antagonized by resveratrol treatment. TLR2 silence significantly attenuated LPS-induced increase TNF-α, IL-1β, IL-6 and IL-8 expression and oxidative stress of granulosa cells. Furthermore, TLR2 overexpression promoted inflammatory response and oxidative stress in the granulosa cells, which was antagonized by resveratrol treatment. In conclusion, resveratrol could attenuate LPS-induced inflammation and oxidative stress in granulosa cells, and the underlying mechanisms may be related to the inhibitory effect of resveratrol on TLR2 expression in granulosa cells.
多囊卵巢综合征（PCOS）是育龄女性常见的内分泌紊乱疾病，但其病理生理学尚未完全阐明。本研究检测了白藜芦醇在PCOS细胞模型中的潜在作用，并探讨了白藜芦醇与Toll样受体2（TLR2）之间的潜在相互作用。本研究对两个微阵列数据集（GSE34526和GSE138518）进行了生物信息学分析。我们发现TLR2是可能与PCOS相关的潜在关键基因之一。进一步检测显示，与对照组相比，PCOS组颗粒细胞中TLR2高表达。体外研究表明，LPS干预导致颗粒细胞中TLR2和促炎介质表达增加，并诱导氧化应激，而白藜芦醇处理可浓度依赖性地拮抗这种作用。TLR2沉默显著减弱LPS诱导的颗粒细胞中TNF-α、IL-1β、IL-6和IL-8表达增加以及氧化应激。此外，TLR2过表达促进颗粒细胞中的炎症反应和氧化应激，而白藜芦醇处理可拮抗这种作用。总之，白藜芦醇可减轻LPS诱导的颗粒细胞炎症和氧化应激，其潜在机制可能与白藜芦醇对颗粒细胞中TLR2表达的抑制作用有关。
