Syringic Acid Extracted from Herba dendrobii Prevents Diabetic Cataract Pathogenesis by Inhibiting Aldose Reductase Activity

• Published in: Evidence-based complementary and alternative medicine Vol. 2012; no. 2012; pp. 1 - 13
• Main Authors: Gu, Lianquan, Wang, Ling, Fang, Hua, Gao, Xinxin, Qi, Hui, Yi, Yanchun, Chen, Dan, Wei, Xiaoyong, Gu, Qiong
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 01.01.2012; Hindawi Limited
• Subjects: Acids; Aldehyde reductase; Animal models; Apoptosis; Cataracts; Chemistry; Chinese medicine; Dendrobium; Dendrobium nobile; Diabetes; Diabetes mellitus; Docking; Drug dosages; Enzymes; Gene expression; Hydrogen bonding; Hydrophobicity; Inhibition; Microscopy; Molecular chains; Pathogenesis; Pharmaceutical sciences; Polymerization; Reductase; Transparency; Turbidity; United States > US; China
• ISSN: 1741-427X; 1741-4288
• DOI: 10.1155/2012/426537

Effects of Syringic acid (SA) extracted from dendrobii on diabetic cataract (DC) pathogenesis were explored. Methods. Both in vitro and in vivo DC lens models were established using D-gal, and proliferation of HLEC exposed to SA was determined by MMT assay. After 60-day treatment with SA, rat lens transparency was observed by anatomical microscopy using a slit lamp. SA protein targets were extracted and isolated using 2-DE and MALDI TOF/TOF. AR gene expression was investigated using qRT-PCR. Interaction sites and binding characteristics were determined by molecule-docking techniques and dynamic models. Results. Targeting AR, SA provided protection from D-gal-induced damage by consistently maintaining lens transparency and delaying lens turbidity development. Inhibition of AR gene expression by SA was confirmed by qRT-PCR. IC50 of SA for inhibition of AR activity was 213.17 μg/mL. AR-SA binding sites were Trp111, His110, Tyr48, Trp20, Trp79, Leu300, and Phe122. The main binding modes involved hydrophobic interactions and hydrogen bonding. The stoichiometric ratio of non-covalent bonding between SA and AR was 1.0 to 13.3. Conclusion. SA acts to prevent DC in rat lenses by inhibiting AR activity and gene expression, which has potential to be developed into a novel drug for therapeutic management of DC.