Tanshinone IIA protects lens epithelial cells from hydrogen peroxide-induced injury. - GreenMedInfo Summary
Tanshinone IIA protects lens epithelial cells from HO-induced injury by upregulation of lncRNA ANRIL.
J Cell Physiol. 2019 Jan 30. Epub 2019 Jan 30. PMID: 30701534
Tanshinone IIA is a lipophilic diterpene extracted from the Salvia miltiorrhiza bunge, possessing antiapoptotic and antioxidant activities. The purpose of this study was to explore the effects of Tanshinone IIA on age-related nuclear cataract. Human lens epithelial cell line SRA01/04 was subjected to HOto mimic a cell model of cataract. Cell Counting Kit-8 assay, flow cytometer, and reactive oxygen species (ROS) detection were performed to evaluate the effect of Tanshinone IIA pretreatment on SRA01/04 cells injured by HO. Besides, the real-time quantitative polymerase chain reaction was used to assess the expression of long noncoding RNA (lncRNA) antisense noncoding RNA in the INK4 locus (ANRIL). Western blot analysis was performed to detect the expression of core proteins involved in cell survival and nuclear factor-κB (NF-κB) pathway. HOsignificantly decreased SRA01/04 cells viability, whereas increased apoptosis and ROS generation. This phenomenon was coupled with the upregulated p53, p21, Bax, cleaved caspase-3, and the downregulated cyclinD1, CDK4, and Bcl-2. Tanshinone IIA pretreatment protected SRA01/04 cells against HO-induced injury. In the meantime, the expression of lncRNA ANRIL was upregulated by Tanshinone IIA. And, the protective effects of Tanshinone IIA on HO-stimulated SRA01/04 cells were abolished when lncRNA ANRIL was silenced. Moreover, the elevated expression of lncRNA ANRIL induced by Tanshinone IIA was abolished by BAY 11-7082 (an inhibitor of NF-κB). To conclude, Tanshinone IIA protects SRA01/04 cells from apoptosis triggered by HO. Tanshinone IIA confers its protective effects possibly via modulation of NF-κB signaling and thereby elevating the expression of lncRNA ANRIL.