Evaluating the protective role of Deglycyrrhizinated licorice root supplement on bleomycin induced pulmonary oxidative damage.

The goal of this study was to investigate the protective effect of licorice supplements in a rat model of Bleomycin-induced lung oxidative damage over a duration of one month. The rats were randomly divided into six groups (n = 10 per group). Control group; Bleomycin group (B): rats were IP injected with bleomycin 5 mg/kg twice weekly. Licorice group (L): rats received orally 300 mg/kg licorice extract. Bleomycin and a low dose of Licorice group (BLLG): rats received orally 75 mg/kg licorice daily and injected as the B group. Bleomycin and a middle dose of Licorice group (BMLG): rats received orally 150 mg/kg licorice daily and injected as the Bleomycin group. Bleomycin and a high dose of Licorice group (BHLG): rats received orally 300 mg/kg licorice daily and injected as the Bleomycin group. Treatment with Bleomycin induced inflammation and oxidative damage to the lungs expressed in the disturbance of the measured parameters in the blood serum, the lung tissue, and the broncholavage fluid. In addition to the decreased expression of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and catalase (CAT) in the lung tissues. Bleomycin caused deformative changes in the histopathological and cellular examination of the lungs especially in the alveolar cells and the interstitial space. On the other hand, treated the bleomycin group with different doses of licorice supplement activates the antioxidant defense mechanism and attenuates the oxidative damage and damage induced to the lung. In conclusion, Deglycyrrhizinated licorice root supplement provided strong antioxidant and protective effects on Bleomycin-induced lung damage.

Cardioactive and vasoactive effects of natural wild honey against cardiac malperformance induced by hyperadrenergic activity.

Induction of hyperadrenergic activity was experimentally achieved in urethane-anesthetized rats using epinephrine (adrenaline). Acute administration of epinephrine (100 microg/kg) for 2 hours induced several cardiac disorders and vasomotor dysfunction. Pretreatment with natural wild honey (5 g/kg) for 1 hour prior to the injection with epinephrine (100 mug/kg) protected the anesthetized normal rats from the incidence of epinephrine-induced cardiac disorders and vasomotor dysfunction. Moreover, posttreatment with natural wild honey (5 g/kg) following the injection with epinephrine (100 microg/kg) for 1 hour showed several ameliorative outcomes to the electrocardiographic parameters and vasomotor dysfunction of anesthetized stressed rats. Furthermore, natural wild honey preserved the positive inotropic effect of epinephrine in both cases. Also, the total antioxidant capacity (AOC) of natural wild honey was found to be very pronounced. Levels of both reduced glutathione and ascorbic acid (vitamin C) were considered relatively high in natural wild honey. Activity of superoxide dismutase (SOD) was also high, whereas catalase activity was relatively low, especially when compared to the value of SOD activity. It would appear from the results of the present study that natural wild honey may exert its cardioprotective and therapeutic effects against epinephrine-induced cardiac disorders and vasomotor dysfunction directly, via its very pronounced total AOC and its great wealth of both enzymatic and nonenzymatic antioxidants involved in cardiovascular defense mechanisms, besides its substantial quantities of mineral elements such as magnesium, sodium, and chlorine, and/or indirectly, via the enhancement of the endothelium-derived relaxing factor nitric oxide release through the influence of ascorbic acid (vitamin C).