Effect of resveratrol on endoplasmic reticulum stress and apoptosis in thyroid follicular cells induced by high iodine
- VernacularTitle:白藜芦醇对高碘诱导的甲状腺滤泡细胞内质网应激和凋亡的影响
- Author:
Yifei ZHANG
1
;
Shuqin LI
;
Zhiyong YANG
Author Information
- Publication Type:Research Article
- Keywords: resveratrol; thyroid follicular cells; iodine excess; endoplasmic reticulum stress; apoptosis
- From: Journal of Clinical Medicine in Practice 2024;28(16):44-48
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of resveratrol on endoplasmic reticulum stress and apoptosis in thyroid follicular cells induced by high iodine. Methods The thyroid follicular cell line Nthy-ori 3-1 was cultured
in vitro and divided into four groups based on different culture methods: normal culture group (Normal group), high iodine group (HI group), resveratrol group (RES group), and high iodine combined with resveratrol group (HI+RES group). Cell proliferation activity was detected by CCK-8 assay, cell apoptosis was detected by TUNEL assay, and theBIP ,CHOP ,IRE1 mRNA expressions were detected by real-time quantitative polymerase chain reaction (PCR). Western blot was used to detect the protein expressions of BIP, CHOP, and IRE1. Results Compared with the Normal group, the proliferation activity of cells in the HI group decreased after 72 hours of culture, the proportion of apoptotic cells increased, the proportion of TUNEL staining positive cells increased, and the relative expressions ofBIP ,CHOP ,IRE1 mRNA, as well as BIP and CHOP proteins were significantly elevated (P < 0.001 orP < 0.05). Compared with the HI group, the proliferation activity of cells in the HI+RES group increased after 72 hours of culture, the proportion of apoptotic cells decreased, the proportion of TUNEL staining positive cells decreased, and the relative expressions ofBIP ,CHOP mRNA, as well as BIP and CHOP proteins, were significantly reduced(P < 0.001 orP < 0.01). Conclusion Resveratrol exerts a protective effect on thyroid follicular cells induced by high iodine, significantly inhibiting endoplasmic reticulum stress and apoptosis caused by excessive iodine intake.