Gallic acid protects against isoproterenol-induced cardiotoxicity in rats

Abstract

Background Gallic acid (GA) is a polyphenolic agent with interesting pharmacological impacts on the cardiovascular system. Objective The present study purposed to study the protective effects of GA at 25 and 50 mg/kg against isoproterenol (ISO)-induced cardiac damage in ischemia/reperfusion (I/R) in rats. Methods Male Wistar rats were randomly assigned into six groups: Control, Control treated with GA at 25 mg/kg (GA25), Control treated with GA at 50 mg/kg (GA50), Hypertrophic rats induced by ISO (ISO), Hypertrophic rats treated with GA at 25 mg/kg (ISO+GA25), and Hypertrophic rats treated with GA at 50 mg/kg (ISO+GA50). Heart isolation was performed to induce a cardiac I/R injury model. Cardiac hemodynamic parameters were recorded. Serum Lactate Dehydrogenase (LDH) and Creatine Kinase-MB (CK-MB) and cardiac Superoxide dismutases (SOD) levels were evaluated. The gene expression of Sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) was assessed. Results We found that GA at 50 mg/kg was significantly increased cardiac function at post I/R period in ISO-induced hypertrophic hearts. Moreover, it suppressed cardiac hypertrophy, the serum LDH and CK-MB levels in ISO injected rats. Administration of GA at 50 mg/kg was significantly increased SOD level and SERCA2a gene expression in the hypertrophic hearts. Conclusion GA at 50 mg/kg could improve cardiac performance possibly by increasing antioxidant defense enzymes, reducing cell damage, and enhancing SERCA2a gene expression in hypertrophic heart induced by ISO in I/R injury conditions.

Mitochondrial biogenesis as an underlying mechanism involved in the cardioprotective effects of Gallic acid against D‐galactose-induced aging

“…GA is a polyphenol that indicates protective effects against cardiac hypertrophy, mitochondrial dysfunction, and oxidative stress in the heart [18,32]. Many evidence indicate that GA has various pharmacologic properties including anti-in ammatory, antioxidant, anti-apoptosis, and antitumor effects [20]. Previous studies of ours indicated many bene cial impacts of the GA at the cardiovascular level [19,20,33].…”

Syringic acid mitigates isoproterenol‐induced cardiac hypertrophy and fibrosis by downregulating Ereg

“…Syringic acid is a 3,5‐dimethyl ether derivative of gallic acid. Gallic acid is reported to alleviate cardiac hypertrophy, fibrosis, cardiotoxicity, hypertension and heart failure 12,22–26 . We hypothesized that syringic acid exerts cardioprotective effects.…”

“…Gallic acid is reported to alleviate cardiac hypertrophy, fibrosis, cardiotoxicity, hypertension and heart failure. 12,[22][23][24][25][26] We hypothesized that syringic acid…”

Cardioprotective potential of vanillic acid

“…Recently, antioxidant consumption has been shown to delay the progression of tissue damage due to drugs 114,115 . There is evidence that phytochemicals that originated from plants or fruits can act as protective agents against ISP‐induced cardiac disorders, particularly those associated with OS 116–118 . Analogously, findings of in vivo study indicated that pretreatment with VA minimizes the leakage of troponin‐ I and T in consequence of damage to myocytes 27 .…”

“…114,115 There is evidence that phytochemicals that originated from plants or fruits can act as protective agents against ISP-induced cardiac disorders, particularly those associated with OS. [116][117][118] Analogously, findings of in vivo study indicated that pretreatment with VA minimizes the leakage of troponin-I and T in consequence of damage to myocytes. 27 ISP administration also induces an increase in ST-segment and a decrease in R-amplitude.…”