Vernonia amygdalina protects against doxorubicin-induced hepatic and renal damage in rats: mechanistic insights

The use of the chemotherapeutic agent doxorubicin is limited due to its potential to cause signifi-cant hepatorenal damage. The present study aimed to investigate the potential hepatoprotective and nephroprotective effects of Vernonia amygdalina, a medicinal plant with known antioxidant and anti-inflammatory properties, against doxorubicin-induced toxicity in rats. Male Wistar rats were randomly divided into four groups: Control, Doxorubicin (DOX), DOX + Vernonia Amyg-dalina (DOX+VA), and Vernonia amygdalina (VA) alone. DOX and DOX+VA groups were treated with a single intraperitoneal injection of doxorubicin (15 mg/kg body weight). The DOX+VA group received Vernonia amygdalina extract (100, 300, 500 mg/kg body weight) by oral gavage for 14 days following doxorubicin injection. The results demonstrated that Vernonia amygdalina significantly reduced the elevated levels of liver and kidney function biomarkers, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and creatinine, induced by doxorubicin. The histological examination of the liver and kidney tis-sues also confirmed the protective effects of Vernonia amygdalina against doxorubicin-induced damage. Furthermore, Vernonia amygdalina treatment was found to mitigate oxidative stress by restoring the levels of glutathione (GPx), Catalase, NO and SOD and decreasing the level of malondialdehyde (MDA) in liver and kidney tissues. Additionally, Vernonia amygdalina sig-nificantly suppressed the renal injury markers, NGAL, cystatin-c, KIM-1, and NAG. In conclu-sion, the results of this study suggest that Vernonia amygdalina has potent hepatoprotective and nephroprotective effects against doxorubicin-induced toxicity in rats. These protective effects are mediated by its antioxidant, and free radical scavenging properties. Further investigation is needed to determine the potential clinical relevance of Vernonia amygdalina in protecting against the hepatorenal damage induced by doxorubicin in human subjects. Graphical abstract

Phytochemical profiling and cardioprotective activity of Vernonia amygdalina ethanol extract (VAEE) against ISO-induced cardiotoxicity in rats

Cardiovascular disorder is the leading cause death in the world, one of them are acute myocardial infarction (AMI) which associated with hypertension and cardiac remodeling. ISO may cause inflammation, enhance the production of oxidative stress while decrease the antioxidant defensive system, myocardium impairment, calcium overload, enhanced cyclic adenosine monophosphate level, intracellular acidosis, and altered membrane permeability. Vernonia amygdalina (VA) is a medicinal plant with antioxidant and anti-inflammatory properties. This study investigated the potential cardioprotective effect of VA on ISO-induced cardiac toxicity in rats. Male Wistar rats were randomly divided into six groups: ISO (ISO), quercetin 100 mg/kg plus ISO (ISO+QR), VA ethanol extract 100, 300, 500 mg/kg plus ISO (ISO+VA100, ISO+VA300 and ISO+VA500). ISO was administered subcutaneously (85 mg/kg) on days 15 while quercetin and VA extract and was given orally for 14 days. At the end of the experiment, the blood was taken from the heart were analyzed for markers of cardiac, oxidative stress and inflammation. The ISO group exhibited significant (p<0.05) elevation of cardiac biomarkers such as lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), troponin-T, and BNP as well as increased oxidative stress markers such as malondialdehyde (MDA) and reduced antioxidant enzyme superoxide dismutase (SOD), catalase (CAT), and Glutathione peroxidases (GPx). Additionally, the ISO group had elevated levels of pro-inflammatory cytokines interleukin-1 (IL-1), interleukin-6 (IL-6), Highly sensitive c reactive protein (HsCRP) and tumor necrosis factor-alpha (TNF-α). Treatment with VA extract significantly (p<0.001) reduced these parameters in the VA+ISO group compared to the ISO group. These findings suggest that VA has a potential protective effect against ISO-induced cardiotoxicity by reducing oxidative stress, apoptosis, and inflammation. (The graphiccal abstract can be seen in the Fig. 1)