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ganoderic acid a protects lens epithelial cells from UVB irradiation and delays lens opacity

Chinese Journal of Natural Medicines 2020年第12期18卷 934-940页

作者： KANG Li-Hua ZHANG Guo-Wei ZHANG Jun-Fang QIN Bai GUAN Huai-Jin Eye Institute Affiliated Hospital of Nantong UniversityNantong 226000China

A contributory role of oxidative stress and protection by antioxidant nutrients have been suspected in cataract *** acid A(GAA),an effective lanostane triterpene,is widely reported as an *** aim of this study is to investigate the potential effects of GAA on cataract *** lens epithelial cells(LECs)were exposed to UVB radiation for different periods,cell viability,apoptosis-related protein levels,malondialdehyde(MDA)and superoxide dismutase(SOD)activities were *** found that cell viability,the Bcl-2/Bax ratio and SOD activity were increased,while Cleaved caspase-3 levels and MDA activity were decreased compared with those in UVB-impaired LECs after GAA ***,GAA activated PI3 K/AKT in UVB-impaired LECs and effectively delayed the occurrence of lens opacity in *** conclusion,these findings demonstrated that GAA exhibited protective functions in SRA01/04 cells and rat lenses against UVB-evoked impairment through elevating cell viability and antioxidant activity,inhibiting cell apoptosis,activating the PI3 K/AKT pathway and delaying lens opacity.

关键词： ganoderic acid a Cataract Lens epithelial cells Cell vitality Apoptosis

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ganoderic acid a ameliorates renalﬁbrosis by suppressing the expression of NPC1L1

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BIOCELL 2024年第11期48卷 1625-1638页

作者： TIANYUN HAN ZHONG LI LUONING ZHANG LINSHEN XIE Department of Nephrology and Environmental Occupational Health West China School of Public Health and West China Fourth HospitalSichuan UniversityChengdu610041China

Objective: The study aimed to explore the protective mechanism of ganoderic acid a (GAA) in renal ﬁbrosisand to verify that GAA can ameliorate renal ﬁbrosis by regulating the Niemann-pick C1-like 1 (NPC1L1) gene. Methods:Transforming growth factor beta1 (TGF-β1) was used to treat Human Kidney-2 (HK-2) cells to establish a renal ﬁbrosismodel. The differentially expressed genes in the control (CTRL) group, TGF-β1 group, and TGF-β1 + GAA group werescreened via transcriptome sequencing technology and veriﬁed by qPCR and Western blot experiments. The NPC1L1gene overexpression plasmid was constructed. The expression levels of N-cad, E-cad, and Slug-related proteins inCTRL, TGF-β1, TGF-β1+GAA (25 μg/mL), and TGF-β1+GAA (25 μg/mL) + NPC1L1 Overexpression (OE) groupswere detected by qPCR and Western blot analysis. Western blot analysis was used to identify the extracellular matrixassociated proteins Tenascin-C, α-SMA, and ﬁbrosis-related protein Collagen I. Fibrosis marker protein Fibronectinwas detected and quantiﬁed by immunoﬂuorescence. Results: Transcriptomic sequencing revealed that TGF-β1stimulation led to 267 differentially regulated genes, with 118 up-regulated and 149 down-regulated, while furthermodulation of 213 genes, comprising 112 up-regulated and 101 down-regulated genes, was observed in the GAAintervention group. The target gene in these processes was found to be NPC1L1 by investigations using GeneOntology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). qPCR and Western blot resultsconﬁrmed that TGF-β1 increased NPC1L1 expression, which was attenuated by GAA. Additionally, TGF-β1upregulated N-cad and Slug. However, GAA reversed this effect and NPC1L1 overexpression partially rescued theGAA effect. TGF-β1 also decreased E-cad expression, reversed by GAA, and NPC1L1 overexpression antagonized thisreversal. Furthermore, TGF-β1 promoted Collagen I, α-SMA, and Tenascin-C expression, and GAA reduced theselevels, effects that were reversed by NPC1L1 ove

关键词： ganoderic acid a NPC1L1 Epithelial-mesenchymal transition Renalﬁbrosis Transcriptomics TGF-β

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