Chemical composition and antimicrobial activity of solidago canadensis linn. Root essential oil.

The essential oil from the roots of Solidago canadensis Linn. (fam. Asteraceae) was analyzed by GC, GC/MS and NMR spectroscopy. Thirty nine constituents comprising 75.4% of the total oil were identified from the oil. Thymol constituted 20.25% of the oil followed by α-copaene (6.26%) and carvacrol (5.51%). The antimicrobial activity of the oil was evaluated using disc diffusion method. Results showed that the oil exhibited significant antibacterial activity against S. feacalis and E. coli whereas it showed moderate antifungal activity against C. albicans.

Effect of curcumin on inflammation and oxidative stress in cisplatin-induced experimental nephrotoxicity.

Nephrotoxicity is a major complication and a dose limiting factor for cisplatin therapy. Recent evidence suggests that inflammation and oxidative stress may contribute to the pathogenesis of cisplatin-induced acute renal failure. Curcumin is claimed to be a potent anti-inflammatory and antioxidant agent. The present study was performed to explore the effect of curcumin against cisplatin-induced experimental nephrotoxicity. Curcumin in the dosages of 15, 30, and 60 mg kg(-1) was administered 2 days before and 3 days after cisplatin administration. Renal injury was assessed by measuring serum creatinine, blood urea nitrogen, creatinine, urea clearance, and serum nitrite levels. Renal oxidative stress was assessed by determining renal malondialdehyde levels, reduced glutathione levels and enzymatic activities of superoxide dismutase and catalase. Systemic inflammation was assessed by tumor necrosis factor-alpha (TNF-alpha) levels. A single dose of cisplatin resulted in marked inflammation (486% rise in TNF-alpha level) and oxidative stress and significantly deranged renal functions as well as renal morphology. The serum TNF-alpha level was markedly reduced in curcumin-treated rats. Curcumin treatment significantly and dose-dependently restored renal function, reduced lipid peroxidation, and enhanced the levels of reduced glutathione and activities of superoxide dismutase and catalase. The present study demonstrates that curcumin has a protective effect on cisplatin-induced experimental nephrotoxicity, and this effect is attributed to its direct anti-inflammatory and strong antioxidant profile. Hence, curcumin has a strong potential to be used as a therapeutic adjuvant in cisplatin nephrotoxicity.

6-Gingerol prevents cisplatin-induced acute renal failure in rats.

BACKGROUND: Nephrotoxicity is a major complication and a dose limiting factor for cisplatin therapy. Recent evidence suggests that enhanced oxidative stress caused by oxygen-centered free radicals may contribute to the pathogenesis of cisplatin-induced acute renal failure. 6-Gingerol is claimed to be a potent antioxidant. The present study was performed to explore the renoprotective potential of 6-gingerol on cisplatin-induced oxidative stress and renal dysfunction. METHODS: 6-Gingerol in dosages of 12.5, 25, 50 mg/kg was administered 2 days before and 3 days after cisplatin administration. Renal injury was assessed by measuring serum creatinine, blood urea nitrogen, creatinine, urea clearance and serum nitrite levels. Renal oxidative stress was assessed by determining renal malondialdehyde levels, reduced glutathione levels and enzymatic activities of superoxide dismutase and catalase. RESULTS: A single dose of cisplatin resulted in marked renal oxidative and nitrosative stress and significantly deranged renal functions. 6-Gingerol treatment significantly and dose-dependently restored renal functions, reduced lipid peroxidation and enhanced the levels of reduced glutathione and activities of superoxide dismutase and catalase. CONCLUSIONS: The present study demonstrates the renoprotective potential of 6-gingerol against cisplatin-induced oxidative stress and renal dysfunction in rats. Hence, 6-gingerol has a potential to be used as therapeutic adjuvant in cisplatin nephrotoxicity.

Renoprotective effect of Spirulina fusiformis on cisplatin-induced oxidative stress and renal dysfunction in rats.

Cisplatin is an effective chemotherapeutic agent used in the treatment of a wide array of both pediatric and adult malignancies. Dose-dependent and cumulative nephrotoxicity is the major toxicity of this compound, sometimes requiring a reduction in dose or discontinuation of treatment. Recent evidences have implicated oxidative and nitrosative stress in cisplatin-induced nephrotoxicity. Spirulina fusiformis, blue-green algae, is claimed to be a potential antioxidant. The present study was designed to explore the renoprotective potential of Spirulina fusiformis against cisplatin-induced oxidative stress and renal dysfunction. Spirulina fusiformis (500,1000,1500 mg/kg(-1) p.o.) was administered 2 days before and until 3 days after cisplatin challenge (5 mg/kg(-1) i.p.). Renal injury was assessed by measuring serum creatinine, blood urea nitrogen, creatinine and urea clearance, and serum nitrite levels. Renal oxidative stress was determined by renal TBARS levels, reduced glutathione levels, and by enzymatic activity of superoxide dismutase and catalase. A single dose of cisplatin produced marked renal oxidative and nitrosative stress and significantly deranged renal functions. Chronic Spirulina fusiformis treatment significantly and dose-dependently restored renal functions, reduced lipid peroxidation, and enhanced reduced glutathione levels, superoxide dismutase, and catalase activities. The results of the present study clearly demonstrate the pivotal role of reactive oxygen species and their relation to renal dysfunction and point to the therapeutic potential of Spirulina fusiformis in cisplatin-induced nephrotoxicity.

Effect of Spirulina, a blue green algae, on gentamicin-induced oxidative stress and renal dysfunction in rats.

Gentamicin (GM), an aminoglycoside, is widely employed in clinical practice for the treatment of serious Gram-negative infections. The clinical utility of GM is limited by the frequent incidence of acute renal failure. Experimental evidences suggest that oxidative and nitrosative stress play an important role in GM nephrotoxicity. Spirulina fusiformis is a blue green algae with potent free radical scavenging properties. The present study was designed to investigate renoprotective potential of S. fusiformis, against GM-induced oxidative stress and renal dysfunction. Spirulina fusiformis (500, 1000, 1500 mg/kg, p.o.) was administered 2 days before and 8 days concurrently with GM (100 mg/kg, i.p.). Renal injury was assessed by measuring serum creatinine, blood urea nitrogen and creatinine clearance and serum nitrite levels. Renal oxidative stress was determined by renal malondialdehyde levels, reduced glutathione levels and by enzymatic activity of superoxide dismutase (SOD) and catalase. Chronic GM administration resulted in marked renal oxidative and nitrosative stress and significantly deranged renal functions. Treatment with S. fusiformis significantly and dose-dependently restored renal functions, reduced lipid peroxidation and enhanced reduced glutathione levels, SOD and catalase activities. The results of present study clearly demonstrate the pivotal role of reactive oxygen species and their relation to renal dysfunction and point to the therapeutic potential of S. fusiformis in GM-induced nephrotoxicity.

Green tea (Camellia sinensis) extract ameliorates endotoxin induced sickness behavior and liver damage in rats.

Immune activation, either by cytokines or endotoxin, elicits a constellation of nonspecific symptoms such as weakness, malaise, listlessness, fatigue, adipsia, anorexia, depression and anxiety collectively termed as sickness behavior. Further, endotoxin administration in animals has been implicated in the pathogenesis of many types of liver disease. Green tea, a common household drink, is rich in antioxidant polyphenols demonstrating inhibitory effects on cytokine production. The present study was designed to investigate the effect of chronic treatment of green tea extract (GTE) on lipopolysaccharide (LPS)-induced sickness behavior and liver damage in rats. The hypothesis was tested through the analysis of LPS-induced behavioral changes in rats, in plus maze and open field paradigms. Other parameters such as feeding and water consumption, weight loss and organ weight index were also estimated. Liver function tests were conducted to investigate the effect of GTE supplementation on LPS-induced hepatic dysfunction. The results of the study demonstrated that GTE significantly attenuated LPS-induced sickness behavior as well as hepatic damage either by its antioxidant activity or by inhibiting LPS induced cytokine production in rats.

Hesperidin, a citrus bioflavonoid, decreases the oxidative stress produced by carbon tetrachloride in rat liver and kidney.

BACKGROUND: CCl4 is a well-established hepatotoxin inducing liver injury by producing free radicals. Exposure to CCl4 also induces acute and chronic renal injuries. The present study was designed to establish the protective effect of hesperidin (HDN), a citrus bioflavonoid, on CCl4-induced oxidative stress and resultant dysfunction of rat liver and kidney. METHODS: Animals were pretreated with HDN (100 and 200 mg/kg orally) for one week and then challenged with CCl4 (2 ml/kg/s.c.) in olive oil. Rats were sacrificed by carotid bleeding under ether anesthesia. Liver enzymes, urea and creatinine were estimated in serum. Oxidative stress in liver and kidney tissue was estimated using Thiobarbituric acid reactive substances (TBARS), glutathione (GSH) content, superoxide dismutase(SOD), and Catalase (CAT) RESULTS: CCl4 caused a marked rise in serum levels of ALT and AST (P < 0.05). TBARS levels were significantly increased whereas GSH, SOD and CAT levels decreased in the liver and kidney homogenates of CCl4 treated rats. HDN (200 mg/kg) successfully attenuated these effects of CCl4 CONCLUSION: In conclusion, our study demonstrated a protective effect of HDN in CCl4 induced oxidative stress in rat liver and kidney. This protective effect of HDN can be correlated to its direct antioxidant effect.