Kidney damage has been associated with administration diclofenac, a phenylacetic acid derivative belonging to the nonsteroidal anti-inflammatory drugs (NSAIDs), which is commonly used for the treatment of various dise...Kidney damage has been associated with administration diclofenac, a phenylacetic acid derivative belonging to the nonsteroidal anti-inflammatory drugs (NSAIDs), which is commonly used for the treatment of various diseases such as rheumatoid arthritis, ankylosing spondylitis, acute muscle pain conditions and osteoarthritis. This study investigated the exact mechanism of diclofenac in renal toxicity by determining the involvement of oxidative stress in rats. Adult male Wistar rats were divided into two groups of eight rats in each group and orogastrically treated for three days. Group 1 served as the normal control and received normal saline (0.9% w/v) and group 2 received 40 mg/kg body weight of diclofenac for three days. Administration of diclofenac caused degeneration of the kidney of rats as evidenced by significant elevation in the serum levels of creatinine, urea, albumin, uric acid, protein and electrolytes and the activities of renal-5’-nucleotidase and glucose-6-phosphate-dehydrogenase (G6PDH) compared with control. Furthermore, administration of diclofenac decreased the activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glutathione-S-transferase (GST) and the level of glutathione with concomitant increase in hydrogen peroxide (H2O2) and malondialdehyde (MDA) levels in the kidney of the diclofenac treated groups compared with control. These findings reveal that administration of diclofenac may impair kidney functions through induction of oxidative stress.展开更多
Hepatic injury has been reported to be associated with chloroquine therapy. Gomphrena celesioides has been claimed to have pleiotropic protective properties in the liver by traditional herbal practitioner but there is...Hepatic injury has been reported to be associated with chloroquine therapy. Gomphrena celesioides has been claimed to have pleiotropic protective properties in the liver by traditional herbal practitioner but there is no scientific evidence to this claim. This investigation therefore sought to evaluate the effect of Gomphrena celesioides administration on chloroquine-induced hepatic injury in rats. Forty adult male rats were divided into five groups of eight rats and were treated orally once daily. Rats in group one received 1 ml/kg body weight of 0.9% normal saline;rats in group two received 250 mg/kg body weight of chloroquine for three days;groups three, four and five rats were pre-treated with 200 mg/kg, 400 mg/kg and 800 mg/kg body weight of methanol extract of Gomphrena celesiodes for three days and on the fourth day were given 250 mg/kg body weight of chloroquine for three days. The experiment lasted for seven days. Liver injury was manifested biochemically by a significant increase in serum level or activities of hepatic markers (aminotransferases, alkaline phosphate, bilirubin, cholesterol and gamma glutamyl transferase). In addition, hepatic tissue from chloroquine-treated rats showed a significant increase in lipid peroxidation with a decrease in hepatic superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase and glutathione reservoirs. Moreover, the liver histopathologic evaluation revealed significant in chloroquine-treated rats. Gomphrena celesioides administration significantly alleviated chloroquine-induced pathologic changes in serum biochemistry and liver tissue. The results also suggest that Gomphrena celesioides possesses protective properties against chloroquine-induced liver injury via mitigation of drug-induced oxidative stress and its consequent events.展开更多
文摘Kidney damage has been associated with administration diclofenac, a phenylacetic acid derivative belonging to the nonsteroidal anti-inflammatory drugs (NSAIDs), which is commonly used for the treatment of various diseases such as rheumatoid arthritis, ankylosing spondylitis, acute muscle pain conditions and osteoarthritis. This study investigated the exact mechanism of diclofenac in renal toxicity by determining the involvement of oxidative stress in rats. Adult male Wistar rats were divided into two groups of eight rats in each group and orogastrically treated for three days. Group 1 served as the normal control and received normal saline (0.9% w/v) and group 2 received 40 mg/kg body weight of diclofenac for three days. Administration of diclofenac caused degeneration of the kidney of rats as evidenced by significant elevation in the serum levels of creatinine, urea, albumin, uric acid, protein and electrolytes and the activities of renal-5’-nucleotidase and glucose-6-phosphate-dehydrogenase (G6PDH) compared with control. Furthermore, administration of diclofenac decreased the activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glutathione-S-transferase (GST) and the level of glutathione with concomitant increase in hydrogen peroxide (H2O2) and malondialdehyde (MDA) levels in the kidney of the diclofenac treated groups compared with control. These findings reveal that administration of diclofenac may impair kidney functions through induction of oxidative stress.
文摘Hepatic injury has been reported to be associated with chloroquine therapy. Gomphrena celesioides has been claimed to have pleiotropic protective properties in the liver by traditional herbal practitioner but there is no scientific evidence to this claim. This investigation therefore sought to evaluate the effect of Gomphrena celesioides administration on chloroquine-induced hepatic injury in rats. Forty adult male rats were divided into five groups of eight rats and were treated orally once daily. Rats in group one received 1 ml/kg body weight of 0.9% normal saline;rats in group two received 250 mg/kg body weight of chloroquine for three days;groups three, four and five rats were pre-treated with 200 mg/kg, 400 mg/kg and 800 mg/kg body weight of methanol extract of Gomphrena celesiodes for three days and on the fourth day were given 250 mg/kg body weight of chloroquine for three days. The experiment lasted for seven days. Liver injury was manifested biochemically by a significant increase in serum level or activities of hepatic markers (aminotransferases, alkaline phosphate, bilirubin, cholesterol and gamma glutamyl transferase). In addition, hepatic tissue from chloroquine-treated rats showed a significant increase in lipid peroxidation with a decrease in hepatic superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase and glutathione reservoirs. Moreover, the liver histopathologic evaluation revealed significant in chloroquine-treated rats. Gomphrena celesioides administration significantly alleviated chloroquine-induced pathologic changes in serum biochemistry and liver tissue. The results also suggest that Gomphrena celesioides possesses protective properties against chloroquine-induced liver injury via mitigation of drug-induced oxidative stress and its consequent events.
