The current study demonstrated that allicin effectively mitigates cardiac oxidative damage, apoptosis and inflammation, induced by acute DOX intoxication. Therefore, allicin could be a promising cytoprotective agent against DOX cardiotoxicity.

The current study was designed to investigate the beneficial role of diosmin, a biologically active flavonoid, against methotrexate- (MTX-) induced hepatic, renal, and cardiac injuries in mice. Male Swiss albino mice received a single intraperitoneal injection of MTX (at 20 mg/kg, body weight) either alone or in combination with oral diosmin (at 50 or 100 mg/kg body weight, for 10 days). Serum was used to evaluate tissue injury markers, while hepatic, renal, and cardiac tissue samples were obtained for determination of antioxidant activity as well as histopathological examination. Diosmin treatment ameliorated the MTX-induced elevation of serum alkaline phosphatase, aminotransferases, urea, creatinine, lactate dehydrogenase, and creatine kinases as well as plasma proinflammatory cytokines (interleukin-1-beta, interleukin-6, and tumor necrosis factor-alpha). Additionally, both diosmin doses significantly reduced tissue levels of malondialdehyde and nitric oxide and increased those of glutathione, glutathione peroxidase, glutathione reductase, glutathione S-transferase, superoxide dismutase, and catalase, compared to the MTX-intoxicated group. Histopathological examination showed that diosmin significantly minimized the MTX-induced histological alterations and nearly restored the normal architecture of hepatic, renal, and cardiac tissues. Based on these findings, diosmin may be a promising agent for protection against MTX-induced cytotoxicity in patients with cancer and autoimmune diseases.

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Objectives To determine the effects of aqueous extract of Alhagi maurorum against the adverse effects including hepato‐nephrotoxicity induced by a broad‐spectrum antibiotic norfloxacin in rats. Methods Adult male albino rats were treated with or without norfloxacin (10 mg/kg) and Alhagi maurorum (300 mg/kg). Serum samples were collected to evaluate liver and kidney function tests, and hepatic and renal tissue samples were obtained to assess antioxidant activity and histopathological examination. Results Alhagi maurorum ameliorated norfloxacin induced elevated levels of serum alkaline phosphatase (ALP), aminotransferases (AST), urea, creatinine, and uric acid. In addition, Alhagi maurorum significantly reduced the tissue levels of malondialdehyde (MDA), and increased glutathione peroxidase (GPx) and superoxide dismutase (SOD) compared to norfloxacin alone treated group. Histological analysis demonstrate that Alhagi maurorum conserved the hepatic and renal tissue damages induced by norfloxacin. Conclusion These findings indicate that Alhagi maurorum aqueous extract possesses a potent antioxidant activity and could be used to attenuate norfloxacin induced oxidative stress and hepatorenal damage in experimental models. Support or Funding Information No funding support This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

This study investigated the potential role of ivabradine (IVN) in the attenuation of doxorubicin (DXR)-induced cardiotoxicity in rats. A total of 28 Swiss-Albino male mice were used, divided into four equal groups: the negative control did not receive any agents ( n = 7), the DXR group received a single dose of DXR 20 mg/kg ( n = 7), the treated group A was pretreated with IVN 5 mg/kg plus DXR ( n = 7), and the treated group B was pretreated with IVN 10 mg/kg plus DXR ( n = 7). The duration of this study was 10 days. Inflammatory biomarkers, including tumor necrosis factor alpha (TNF-α), lactate dehydrogenase (LDH), malondialdehyde (MDA), and cardiac troponin (cTn-I) serum levels were measured. TNF-α, LDH, MDA, and cTn-I serum levels were higher in the DXR-treated mice compared with the control ( P ˂0.01). IVN produced a dose-dependent effect in the reduction of MDA and cTn-I compared to DXR-treated mice ( P ˂0.05). Our findings suggest that IVN is an effective agent in mitigating DXR-induced cardiotoxicity due to its anti-inflammatory and antioxidant effects. IVN illustrated a dose-dependent effect in the attenuation of DXR-induced cardiotoxicity through inhibition of lipid peroxidation and cardiomyocyte injury.