Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

3, 4-Dihydroxyphenylethanol attenuates cadmium-induced oxidative stress, inflammation and apoptosis in rat heart

Yan Huang¹ , Hongsheng Gang², Bitao Liang³, Ming Li¹

¹Department of Emergency; ²Department of Vasculocardiology, Wuhan Fourth Hospital (Puai Hospital),Tongji Medical College, Huazhong University of Science and Technology; ³Changjiang Polytechnic, Wuhan 430073, Hubei, China.

For correspondence:- Yan Huang Email: holstermarobit@yahoo.com Tel:+862783914556

Accepted: 17 March 2019 Published: 30 April 2019

Citation: Huang Y, Gang H, Liang B, Li M. 3, 4-Dihydroxyphenylethanol attenuates cadmium-induced oxidative stress, inflammation and apoptosis in rat heart. Trop J Pharm Res 2019; 18(4):713-719 doi: 10.4314/tjpr.v18i4.5

© 2019 The authors.
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Abstract

Purpose: To investigate the therapeutic effect of 3, 4-dihydroxyphenylethanol (DOPET) on cadmium (Cd) induced cardiotoxicity in murine model.

Methods: Four groups of rats were used in this study (n = 6). The rats were treated with DOPET and Cd for 28 days. Biochemical parameters were determined in plasma and heart tissue homogenates.

Results: Cadmium (Cd) significantly increased lipid peroxidation and protein carbonylation. However, DOPET treatment significantly attenuated Cd-induced oxidative stress. Cd intoxication significantly increased cardiac markers {creatine kinase, lactate dehydrogenase (LDH) and cardiac troponin-I} levels in plasma, and reduced the levels of antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase Gpx ,glutathione (GSH) and malndialdehyde (MDA) in heart tissue. These Cd-induced changes in cardiac markers and antioxidants were reversed by DOPET treatment. Cd treatment led to upregulation of protein expressions of pro-inflammatory cytokines (TNF-α and Il-6). However, DOPET supplementation brought about a decrease in the protein expressions of these cytokines. Western blot analysis revealed that Cd induced apoptosis in cardiac tissue, as was evident from alterations in protein expressions of the apoptotic inducers, Bax and cleaved caspase-3, and the anti-apoptotic factor Bcl-2. However, DOPET treatment effectively reversed Cd-induced apoptosis.

Conclusion: These results indicate that DOPET exerts cardio-protective effect against Cd-induced toxicity via antioxidant, anti-inflammatory and anti-apoptotic mechanisms.

Keywords: Cadmium, Cardiotoxicity, DOPET, Antioxidant, Inflammation, Apoptosis