The histopathological and molecular protective effects of sinapic acid against lead acetate-induced cardiac damage via NRF2/HO-1 and ER stress-related pathways.

BACKGROUND

Lead acetate (PbAc) is a significant source of threat to living organisms and the environment due to severe industrial exposure. Sinapic acid (SA) exhibits immunomodulatory, antiapoptotic, anticancer, and antioxidant properties. This study investigated the effects of SA on oxidative stress, inflammation and apoptosis in the hearts of rats exposed to PbAc, and its possible protective mechanisms.

METHODS

Thirty-five male Sprague Dawley rats were divided into five groups as control, SA, PbAc, PbAc + SA 5 and PbAc + SA 10. Lead acetate (30 mg/kg) and sinapic acid (5 mg/kg or 10 mg/kg) were administered by gavage to the PbAc and PbAc + SA groups for 7 days.

RESULTS

The results showed that SA prevented the PbAc-induced increase in MDA levels, decrease in GSH, NRF2, HO-1, NQO1 levels and decrease in antioxidant enzyme activities. Additionally, it was observed that the administration of SA alleviated PbAc-induced ER stress by suppressing the expression of the biomarkers CHOP, ATF-6, IRE1, PERK and GRP-78. In rats exposed to PbAc, the levels of apoptotic Bax, Caspase-3, Apaf 1, p53, Caspase-6 and Caspase-9 increased, but the levels of antiapoptotic Bcl-2 decreased. SA treatment showed antiapoptotic effect and regulated apoptotic and antiapoptotic protein levels. Additionally, SA treatment modulated the levels of cardiac markers (LDH, CKMB, troponin-I) and histopathological changes.

CONCLUSION

As a result, it was observed that PbAc had a toxic effect on the cardiac tissue of rats, and it was determined that SA treatment could alleviate this toxicity.