PMID- 31811113 OWN - NLM STAT- MEDLINE DCOM- 20200521 LR - 20200521 IS - 1643-3750 (Electronic) IS - 1234-1010 (Print) IS - 1234-1010 (Linking) VI - 25 DP - 2019 Dec 7 TI - Protective Effect of beta-Glucogallin on Damaged Cataract Against Methylglyoxal Induced Oxidative Stress in Cultured Lens Epithelial Cells. PG - 9310-9318 LID - 10.12659/MSM.917869 [doi] AB - BACKGROUND ss-glucogallin (GG) is one of the major plant polyphenolic antioxidants that have been associated with positive effects on human health and are crucial in the developing defense mechanism against the risk of diseases. However, reports on the protective mechanism of GG in lens epithelial cells are limited. MATERIAL AND METHODS ARPE-19 cells (a human retinal epithelial cell line) were exposed to methylglyoxal (MG) with or without GG to illuminate the protective role of GG in counteracting the cataract signaling. RESULTS Cells predisposed to MG demonstrated an increase in oxidative stress with augmented (P<0.01) inflammatory cytokines such as cyclooxygenase (COX)-2, chemokine receptor CXCR4, interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1 (MCP-1), and intercellular adhesion molecule 1 (ICAM-1) genes. In addition, the expression of aldose reductase (AR) was increased to 2-fold with accumulated sorbitol in MG exposed cells compared to control. On the other hand, cells exposed to MG evidenced a 3-fold increase in RAGE (receptor for advanced glycation end products) and a 2-fold increase in NF-kappaB (nuclear factor kappa-light-chain-enhancer of activated B cells) expression compared to control cells. Intriguingly, lens epithelial cells pre-treated with GG attenuated the reactive oxygen species levels with improved antioxidant enzymes. Simultaneously, the levels of AR and other inflammatory cytokines were observed in the levels closer to control cells in GG pre-treated cells. CONCLUSIONS Thus, the results of the present investigation show that GG may be a potential drug for the prevention of cataract development and progression. FAU - Ma, Ying AU - Ma Y AD - Department of Ophthalmology, The Second Hospital of Dalian Medical University, Dalian, Liaoning, China (mainland). FAU - Liu, Fei AU - Liu F AD - Department of Ophthalmology, The Second Hospital of Dalian Medical University, Dalian, Liaoning, China (mainland). FAU - Xu, Yanli AU - Xu Y AD - Department of Ophthalmology, The Second Hospital of Dalian Medical University, Dalian, Liaoning, China (mainland). LA - eng PT - Journal Article DEP - 20191207 PL - United States TA - Med Sci Monit JT - Medical science monitor : international medical journal of experimental and clinical research JID - 9609063 RN - 0 (Antioxidants) RN - 0 (Chemokine CCL2) RN - 0 (Chemokines) RN - 0 (Cytokines) RN - 0 (Glycation End Products, Advanced) RN - 0 (Hydrolyzable Tannins) RN - 0 (Interleukin-6) RN - 0 (NF-kappa B) RN - 0 (Reactive Oxygen Species) RN - 126547-89-5 (Intercellular Adhesion Molecule-1) RN - 58511-73-2 (glucogallin) RN - 722KLD7415 (Pyruvaldehyde) SB - IM MH - 3T3 Cells MH - Animals MH - Antioxidants/pharmacology MH - Cataract/*drug therapy MH - Cell Line MH - Chemokine CCL2/metabolism MH - Chemokines/metabolism MH - China MH - Cytokines/metabolism MH - Epithelial Cells/metabolism MH - Glycation End Products, Advanced MH - Humans MH - Hydrolyzable Tannins/metabolism/*pharmacology MH - Intercellular Adhesion Molecule-1/genetics MH - Interleukin-6/metabolism MH - Lens, Crystalline/*drug effects/metabolism MH - Mice MH - NF-kappa B/metabolism MH - Oxidative Stress/drug effects/physiology MH - Pyruvaldehyde/pharmacology MH - Reactive Oxygen Species/metabolism MH - Signal Transduction/drug effects PMC - PMC6916131 COIS- Conflicts of interest None. EDAT- 2019/12/08 06:00 MHDA- 2020/05/22 06:00 PMCR- 2019/12/07 CRDT- 2019/12/08 06:00 PHST- 2019/12/08 06:00 [entrez] PHST- 2019/12/08 06:00 [pubmed] PHST- 2020/05/22 06:00 [medline] PHST- 2019/12/07 00:00 [pmc-release] AID - 917869 [pii] AID - 10.12659/MSM.917869 [doi] PST - epublish SO - Med Sci Monit. 2019 Dec 7;25:9310-9318. doi: 10.12659/MSM.917869.