Arabian Primrose (Arnebia hispidissima) is a medicinally and pharmaceutically significant plant. It is broadly dispersed in the North Africa, Egypt, and towards North India. The roots of this plant are thought to be useful in the treatment of headache, fever, tongue and throat diseases in addition to cardiac disorders1. Plants of Arnebia spp. have antifungal, anti-inflammatory, wound-healing and anti-microbial properties2.
Cardio-toxicity and Nephro-toxicity are closely interconnected and illness of one organ cause disturbance in other, lastly leading to the failure of both organs. Cardio-toxicity engross a wide range of cardiac changes from small variations in blood pressure and irregular heart beat to different heart muscle diseases. Nephro-toxicity is a kidney specific disorder in which excretion does not go smoothly owing to toxic chemicals or drugs3.
Substantial reports have demonstrated that exposure to Carbon tetra Chloride (CCl4) induces tissue damage in many organs including brain, kidney, testis, heart and lungs. CCl4 induced heart and kidney damage was connected with the generation of free radicals4.
The protective effect of some plants against CCl4-induced cardio- and nephrotoxicity has been illustrated in many studies5. Recently scientists had studied the protective ability of desert campion plant against CCl4 intoxication by repairing the cardiac and kidney function abnormalities5.
Scientists are checking various plants for their protective effects against kidney and heart disease. So keeping in view the above mentioned facts researchers studied the protective effects of Arnebia hispidissima extract (AHE) on carbon tetrachloride (CCl4)-induced cardiotoxicity and nephrotoxicity6.
The research was conducted on rat model. Adult rats were divided into 5 groups. Heart damage and renal function markers were assessed. Markers of oxidative stress in the cardiac and renal tissues were also estimated by determining the levels of SOD (superoxide dismutase), GPx (glutathione peroxidase), CAT (catalase), GSH (reduced glutathione) and MDA (malondialdehyde). Heart and kidney tissues were investigated for histo-pathological changes.
It was observed that addition of CCl4 notably amplified the levels of cardiac and renal damage markers. Co-administration of CCl4 + AHE significantly calmed the adverse effect of CCl4 in rat and reduced the increased serum levels of cardiac and renal damage markers. AHE remunerated the shortfalls in the antioxidant defense mechanisms (SOD, GPx and CAT) and suppressed LPO (lipid per-oxidation) in rat heart and kidney resulting from CCl4 administration. Moreover, histo-pathological changes induced with CCl4 in heart and kidney tissues of rat were also reduced with the co-administration of AHE.
After the study it was established that oral administration of AHE prevented CCl4-induced cardio- and nephrotoxicity by accelerating heart and kidney antioxidant defense mechanisms and down regulating the LPO near to the normal levels.
Written by: Rabeeia
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