Format

Send to

Choose Destination
Int J Med Sci. 2019 May 10;16(5):729-740. doi: 10.7150/ijms.32222. eCollection 2019.

Protective Effects of Rosmarinic Acid against Selenite-Induced Cataract and Oxidative Damage in Rats.

Author information

1
Department of Applied Cosmetology, National Tainan Junior College of Nursing, Tainan, Taiwan.
2
Department of Biotechnology, TransWorld University, Yunlin County, Taiwan.
3
Department of Optometry, Da-Yeh University, Changhua, Taiwan.

Abstract

Cataracts are the major cause of blindness and are associated with oxidative damage of the lens. In the present study, the aim was to evaluate the protective effects of rosmarinic acid on selenite-induced cataractogenesis in Sprague-Dawley rat pups. The animals were randomly divided into five groups, each of which consisted of 10 rat pups. Group I served as normal control (vehicle administration). For testing cataract induction, animals of Groups II, III, IV, and V were administered a single subcutaneous injection of sodium selenite (2.46 mg/kg body weight) on postpartum day 12. After sodium selenite intoxication, Group II served as control selenite. From the 11th day through the 17th day, Groups III-V received rosmarinic acid intraperitoneally at doses of 5, 10, and 50 mg/kg, respectively. On postpartum day 24, the rat pups were examined for cataract formation, and the lenses were isolated for further analysis of proteins and oxidative damage indicators. Selenite caused significant (p < 0.05) cataract formation. Through the effects of selenite, the protein expressions of filensin and calpain 2 were reduced, and the calcium concentrations, the level of lipid peroxidation (TBARS), and inflammation indicators (iNOS, COX-2, and NFκB) were upregulated. Furthermore, the protein expression of the antioxidant status (Nrf2, SOD, HO-1, and NQO1), the antioxidant enzymes activities (GSH-Px, GSH-Rd, and catalase), and the GSH levels were downregulated. In contrast, treatment with rosmarinic acid could significantly (p < 0.05) ameliorate cataract formation and oxidative damage in the lens. Moreover, rosmarinic acid administration significantly increased the protein expressions of filensin, calpain 2, Nrf2, SOD, HO-1, and NQO1, the antioxidant enzymes activities, and the GSH level, in addition to reducing the calcium, lipid peroxidation, and inflammation indicators in the lens. Taken together, rosmarinic acid is a prospective anti-cataract agent that probably delays the onset and progression of cataracts induced by sodium selenite.

KEYWORDS:

cataractogenesis; oxidative damage; rosmarinic acid; sodium selenite

Conflict of interest statement

Competing Interests: The authors have declared that no competing interest exists.

Supplemental Content

Full text links

Icon for Ivyspring International Publisher Icon for PubMed Central
Loading ...
Support Center