Protective effect of dendropanoxide against cadmium-induced hepatotoxicity via anti-inflammatory activities in Sprague-Dawley rats

Abstract

Cadmium (Cd) accumulates in the body through contaminated foods or water and causes pathological damage to the liver via oxidative stress and inflammatory reactions. This study was conducted to explore the effects of dendropanoxide (DPx) on Cd-induced hepatotoxicity in rats. Sprague-Dawley (SD) rats were injected with CdCl2 (7 mg/kg body weight) intraperitoneally for 14 days for the induction of liver dysfunction. The CdCl2-exposed rats were subjected to DPx (10 mg/kg) or silymarin (50 mg/kg). The animals were euthanized after 24 h of the last CdCl2 injection and the serum biochemical parameters, lipid content, pro-inflammatory cytokine levels, apoptotic cell death and histopathology of the tissues were analyzed. Additionally, the activity of antioxidant enzymes, including superoxide dismutase (SOD) and catalase (CAT), was measured. Compared to controls, Cd-injected rats showed significantly elevated serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglycerides (TG), total cholesterol, and pro-inflammatory cytokines, and a remarkable decrease in SOD and CAT activities. Importantly, Cd-induced liver damage was drastically ameliorated by treatment with DPx or silymarin. Treatment with DPx protected the Cd-induced histopathological hepatic injury, as confirmed by the evaluation of TUNEL assay. DPx treatment significantly reduced Bax and caspase-3 expression in Cd-injected rats. Additionally, HO-1 and NRF2 expressions were significantly increased after DPx administration in the liver of Cd-injected rats. Our data indicate that DPx successfully prevents Cd-induced hepatotoxicity by emphasizing the antioxidant and anti-inflammatory effect.

Graphical Abstract

Keywords:

• Cadmium
• dendropanoxide
• hepatoxicity
• pro-inflammation

Acknowledgements

The author(s) disclose receipt of the following financial support for the research, authorship, and/or publication of this article. The authors would like to acknowledge Korea Brain Korea 21 project.

Authors’ contributions

Sreevarsha Gali, Swati Sharma, Amit Kundu, and Hyung Sik Kim contributed to the conception and design of the study, the acquisition, analysis, and interpretation of data, and drafted; Eunah Lee, Joo Hee Han, Joo Kyung Shin, and So Young Kyung, contributed to data acquisition and analysis; Sreevarsha Gali, Swati Sharma, Ji Soo Choi, and Amit kundu contributed to the data analysis and critical revision of the manuscript; Jae-Sung Kim and Hyung Sik Kim contributed to critical revision of the manuscript; All authors gave final approval and agree to be accountable for all aspects of work, ensuring integrity and accuracy.

Disclosure statement

No potential conflict of interest was reported by the author(s). The authors alone are responsible for the content and writing of this article.

Additional information

Funding

The author(s) reported there is no funding associated with the work featured in this article.