Protective effect of curcumin and gingko biloba l. extract against gentamicin-induced nephrotoxjcity in rats

Gentamicin [GENT] which is a commonly used antibiotic causes nephrotoxicity in man and animals. Generation of free radicals in the renal cortex plays an important role in the pathogenesis of gentamicin-induced nephrotoxicity in rats. Curcumin, the yellow curry pigment isolated from turmeric [the ground rhizome of Curcuma longa L] and Ginkgo biloba extract have been reported to possess antioxidant and free radical scavenging properties. The present study was designed to investigate the potential protective role of curcumin, Ginkgo biloba extract, and their combination on gentamicin-induced nephrotoxicity in rats. The rats were divided into six groups, 8 animals each. Group 1 rats were treated with GENT [80 mg/kg/day] IM for 6 days. Rats of groups 2, 3, and 4 "were pretreated orally for 4 days with curcumin [200 mg/kg/day], Ginkgo biloba leaf extract [300 mg/kg/day], and a combination of curcumin and Ginkgo biloba leaf extract, respectively before concomitant administration of GENT for additional 6 days. Control groups of animals were treated with pure vehicles IM or orally. Nephrotoxicity was evaluated biochemically and histopathologically. Treatment of rats with GENT produced elevation in serum creatinine, urea levels and severe tubular necrosis. Concomitantly, treatment of rats with GENT produced elevation in serum nitrite level, decrease in renal intracellular reduced glutathione [GSH] level and superoxide dismutase [SOD] activity. Pretreatment of rats with curcumin, Ginkgo biloba extract, or their combination decreased GENT-induced disturbances in kidney function and structure. In addition, pretreatment of rats with curcumin, Ginkgo biloba extract, or their combination decreased GENT-induced alterations in serum nitrite level, renal intracellular GSH level and SOD activity. The combined treatment was more effective than either agent alone. These results indicate that curcumin, Ginkgo biloba extract, or their combination has the ability to protect against GENT-induced nephrotoxicity. Inhibition of oxidative stress and nitric oxide production may play an important role in these protective effects

effect of melatonin on pentraxin-3 level and nuclear factor-kappa beta immunohistochemical expression on acetic acid-induced colitis and their relationship to pathophysiology of the disease

Taking into consideration the presence of melatonin [MEL] in gastrointestinal [GI] tissue and its role in gastrointestinal tract [GIT] physiology, it is practical to speculate that melatonin could influence inflammation-related GI disorders, including ulcerative colitis [UC]. We hypothesized the preventive, short and long term effects of melatonin administration on acetic acid [AA] induced colitis in rats and its potential underlying mechanism. We evaluate the immunohistochemical expression of nuclear factor NF-kappa beta [NF-kappa beta]. We also estimated the relation between AA-induced colitis and pentraxin-3 [PTX-3] serum level. The animals were divided into 5 groups. Control group, AA-induced-colitis group, Pre-treated group, Short-term treated group, and Long-term treated group. At the end of the experiment, blood samples were taken for measurement of PTX-3, lipid peroxide [LP] and total thiols [TT]. Colon was taken for histopathological examination and immunohistochemical study for detection of NF- kappa beta expression. MEL is effective in prevention and short-term treatment of AA-induced colitis as indicated by attenuating the colitis symptoms such as rectal bleeding, reduction of the body weight, the increase in the colonic weight and reduction of the severity of mucosal damage dramatically. MEL administration, also decreased NF- kappa beta immunohistochemical expression, decreased serum level of LP and PTX-3 and increased serum level of TT. However, in long-term treatment MEL has negative effect on AA-induced colitis. MEL is effective in prevention and short-term treatment of colonic inflammatory process while long-term treatment exacerbate the colitis. The outcome also indicated that melatonin contributes in a variety of guard mechanisms against colonic inflammatory processes by inhibiting the NF- kappa beta and conserving the vital endogenous antioxidant reserve of TT, thus dipping the level of colonic damage, mainly in the early phase of colitis