Effects of sodium hydrosulfide (NaHS) on cisplatin-induced hepatic and cardiac toxicity

Abstract

In recent years, the cardiotoxicity and hepatotoxicity induced by chemotherapeutic drugs such as cisplatin (CP) have become significant issues. The current research looks into the effects of sodium hydrosulfide (NaHS) on CP-induced hepatotoxicity and cardiotoxicity in rats. A total of 32 male Sprague Dawley rats were separated into four different groups: (1) control group, received only normal saline; (2) NaHS group, was intraperitoneally injected with NaHS (200 µg/kg/d, dissolved in saline) for 15 days; (3) CP group, was intraperitoneally injected only one dose of CP (5 mg/kg) and (4) CP plus NaHS group, received CP along with NaHS. Blood and tissues samples were harvested for biochemical, histopathological, and immunohistochemical investigations. To determine the data’s statistical significance, a one-way analysis of variance was used. CP injection significantly increased alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), Creatine phospho kinase (CK-MB), cholesterol, low-density lipoprotein (LDL), triglyceride (TG), and lipid peroxidation levels, while high-density lipoprotein (HDL), albumin, glutathione peroxidase, superoxide dismutase, and catalase (CAT) levels were significantly reduced with pathological alterations in liver and heart tissues. Co-treatment NaHS with CP ameliorates the biochemical and histological parameters. Also, Treatment solely with CP resulted in increased tissue expression of interleukin-1β (IL-1β) in liver and heart but co-treatment NaHS with CP reduced the expression of this inflammatory factor. We conclude that NaHS operates in the liver and heart as an anti-inflammatory and powerful free radicals’ scavenger to inhibit the toxic effects of CP, both at the biochemical and histopathological levels.

Key Messages

NaHS protects the liver and heart against Cisplatin-induced toxicity

Keywords:

• Cisplatin
• hepatotoxicity
• cardiotoxicity
• sodium hydrosulfide
• oxidative stress
• IL-1β

Acknowledgment

The manuscript has been read and approved by all the authors, that the requirements for authorship as stated earlier in this document have been met, and that each author believes that the manuscript represents honest work. Any limitation is not in the current study, because during the experiment, no deaths were noted in the groups.

Ethical approval

All experimental protocols in the present study were approved by the Ethics Committee on Animal Research of Ahvaz Jundishapur University of Medical Science (Reference Number: IR AJUMS.ABHC. REC.1397.011) in accordance with guidelines of National Institutes of Health (NIH Publications No. 8023, revised 1978).

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

Data will be shared upon request.

Additional information

Funding

This work was supported by grant from Deputy of Research and Technology Development of Ahvaz Jundishapur University of Medical Sciences.