Herbal medicines have been used since the dawn of civilization to maintain health and to treat diseases. Diabetes mellitus is one of the leading cause of death in many developed countries. The incidence of diabetes is increasing at an alarming rate in India. It was estimated that India which had 19.4 million diabetes in 1995 is expected to register a near threefold increase by. Many plants reported to be useful for the treatment of diabetes mellitus in ayurvedic medicine, are being tested for their hypoglycemic activity in experimental animals Lagerstroemia flos- reginae is one such plant commonly found as shade trees in Kerala. In Ayurveda both root and leaves are used in the treatment of diabetes. The main objective of this study was to assess the antidiabetic effect of the alcohol extracted leaves of Lagerstroemia flos- reginae in alloxan induced diabetic rats in terms of controlling blood glucose level, lipid profile, bilirubin, uric acid in serum and lipid peroxides and glutathione in the liver of the experimental animals. The present study has been undertaken to observe the protective effect of the active constituents of Lagerstroemia flos- reginae leaf extracts against alloxan induced diabetes in experimental animal model. The activity of the active constituents was compared with Daonil -a standard drug.
This study evaluated the effect of $\alpha$-tocopherol ($\alpha$-TC), ischemic preconditioning (IPC) or a combination on the extent of mitochondrial injury caused by hepatic ischemia/reperfusion (I/R). Rats were pretreated with $\alpha$-TC (20 mg/kg per day, i.p.) for 3 days before sustained ischemia. A rat liver was preconditioned with 10 min of ischemia and 10 min of reperfusion, and was then subjected to 90 min of ischemia followed by 5 h or 24 h of reperfusion. I/R increased the aminotransferase activity and mitochondrial lipid peroxidation, whereas it decreased the mitochondrial glutamate dehydrogenase activity. $\alpha$-TC and IPC individually attenuated these changes. $\alpha$-TC combined with IPC ($\alpha$-TC+IPC) did not further attenuate the changes. The mitochondrial glutathione content decreased after 5 h reperfusion. This decrease was attenuated by $\alpha$-TC, IPC, and $\alpha$-TC+IPC. The significant production of peroxides observed after 10 min reperfusion subsequent to sustained ischemia was attenuated by $\alpha$-TC, IPC, and $\alpha$-TC+IPC. The mitochondria isolated after I/R were rapidly swollen. However, this swelling rate was reduced by $\alpha$TC, IPC, and $\alpha$-TC+IPC. These results suggest that either $\alpha$-TC or IPC reduces the level of mitochondrial damage associated with oxidative stress caused by hepatic I/R, but $\alpha$- TC combined with IPC offers no significant additional protection.
Sharma, Manju;Anwer, Tarique;Pillai, K K;Haque, Syed Ehtaishamul;Najmi, A K;Sultana, Yasmin
Advances in Traditional Medicine
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v.8
no.2
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pp.146-153
/
2008
The present study is aimed at finding the influence of silymarin (a flavonoid) (25 mg/kg & 50 mg/kg) in streptozotocin (STZ)-induced diabetic rats. Type 2 diabetes was induced by single intraperitoneal injection of STZ (100 mg/kg) to 3 days old rat pups. Silymarin was administered for 15 days after the animals were confirmed diabetic (75 days after STZ injection). Blood glucose, glycosylated hemoglobin ($HbA_{1c}$), lipid peroxides (LPO) levels and reduced glutathione (GSH) contents in pancreas and liver were estimated following the established procedures. Biochemical observations were further substantiated with histological examination of pancreas. Blood glucose and $HbA_{1c}$ levels, which were elevated by STZ, were lowered to physiological levels by the administration of silymarin. The levels of LPO were significantly increased in STZ-induced diabetic rats. Silymarin reduced the LPO levels in both pancreas and liver. GSH contents which were reduced significantly in pancreas and liver of STZ-induced diabetic rats were brought back to near normal levels by silymarin treatment. Multifocal necrotic and degenerative changes of pancreas in STZ-diabetic rats were minimized to near normal morphology by administration of silymarin as evident by histopathological examination. Silymarin showed a dose dependent protective effect on STZ-induced $\beta$-cell damage. It could be attributed to the antioxidative and free radicals scavenging properties of the flavonoid. Thus, it may be considered as a natural antioxidant with potential therapeutic application in the treatment of type 2 diabetes.
To achieve a better understanding of antioxidant action manifested by malotilate, the dithiol malonates, we monitored the oxy radical-scavenging system against the chronic hepatic damage induced by $CCl_4$ alone or in combination with ethanol. Malotilate was given orally at a dose of 100 mg/kg/day and $CCl_4$ 1.5 ml/kg was injected subcutaneously twice a week for 4 weeks. In each group receiving ethanol, drinking water was replaced by 20% aqueous solution or glucose, isocaloric amounts of ethanol, as a control of ethanol was diluted in its drinking water. Each rat was killed as a starved state at 18 hours after the period of the experiment, four weeks. The results were summarized as follows: 1) Malotilate inhibited the rate of generation of superoxide radicals, the accumulation of lipoperoxides, and promoted the synthesis of glutathione in the liver. 2) Malotilate stimulated the enhancement of activity of superoxide dismutase in hepatic mitochondria. 3) Malotilate had no effects on the hepatic $H_2O_2$ contents. 4) Malotilate showed the increase of catalase activity in the liver poisoned with $CCl_4$, and also gave a tendency to increase it in the liver intoxicated with ethanol. Thus, our data suggested that the activation of hepatic antioxidant system in the presence of malotilate would play a role in protecting liver against the toxic effects of oxy radical and/or lipid peroxides under the hepatotoxic conditions induced by $CCl_4$ with or without ethanol. However, the effects of malotilate against the ethanol-induced hepatotoxicity appear to be insignificant.
Mansour, Mahmoud A.;Al-Shabanah, Othman A.;El-Khashef, Hassan A.
BMB Reports
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v.36
no.4
/
pp.373-378
/
2003
Effects of L-arginine and NG-nitro-L-arginine methyl ester (L-NAME) on the renal dysfunction that is induced by cisplatin (CDDP) were investigated. A single dose of CDDP (7.5 mg/kg i.p.) induced renotoxicity, which was manifested by increasing the sensitivity of isolated urinary bladder rings to acetylcholine (ACh), together with a significant elevation of serum urea and creatinine, and a severe decrease in serum albumin. Moreover, renal dysfunction was further confirmed by a significant decrease of enzyme activities, such as glutathione peroxidase, GSH-Px (E.C 1.11.1.9), catalase (E.C 1.11.1.6), as well as a significant increase in lipid peroxides that were measured as malondialdhyde (MDA) in kidney tissue homogenates. The administration of L-arginine (70 mg/kg/d p.o in drinking water 5 d before and 5 d after the CDDP injection) significantly ameliorated the renotoxic effects of CDDP, as judged by restoring the normal responses of isolated bladder rings to Ach, and also by an improvement in a range of renal function indices, which included serum urea and creatinine concentrations and kidney weight. In addition, L-arginine prevents the rise of MDA, as well as a reduction of GSH-Px and catalase activities in kidney tissues homogenates. On the other hand, the administration of L-NAME (4 mg/kg/d p.o) resulted in no protection against renal dysfunction that was induced by CDDP treatment. The findings of this study suggest that L-arginine can attenuate kidney injury that is produced by CDDP treatment. In addition, L-arginine may be a beneficial remedy for CDDP-induced renal toxicity, and could be used to improve the therapeutic index of CDDP.
This study was performed to investigate the effect of dietary $\beta$-carotene supplementation on lipid peroxide levels and antioxidant enzyme activities in alcoholic fatty liver rats. Forty five Sprague-Dawley male rats aging 8 weeks were used as experimental animals, which were divided into the control diet (CD) and the ethanol diet (ED) and the ethanol + $0.02\%$$\beta$-carotene diet (EPD) groups and fed the experimental diet respectively for 5 weeks. After the feeding, rats were sacrificed to get blood and liver to analyze lipid and lipid peroxide levels and antioxidant enzyme activities. The mean body weight and food intake of the ethanol diet group was significantly lower than that of the control diet. The liver index (LI) of the ethanol diet group was significantly higher than those of the control diet and the $\beta$-carotene supplementation group. Serum levels of total lipid, triglyceride of the ethanol diet group were significantly higher than those of the control diet and the $\beta$-carotene supplementation group. Total cholesterol levels were not significantly different among all groups. HDL-cholesterol of the ethanol diet group was significantly lower than those of the control diet and the $\beta$-carotene supplementation group. Liver TBARS of the ethanol diet group was significantly higher than those of the control diet and the $\beta$-carotene supplementation group. Liver lipofuscin and conjugated diene levels were not significantly different among all groups. The superoxide dismutase activity of the ethanol diet group was significantly lower than those of the control diet and the $\beta$-carotene supplementation group. Catalase and glutathione peroxidase activities were not significantly different among all groups. Because v-carotene supplementation significantly decrease the serum total lipid, triglyceride, liver TBARS revels and increase the superoxide dismutase activity in alcoholic ratty liver rats, $\beta$-carotene supplementation seems to give beneficial effect for the alcoholics.
To compare antioxidant action of u 3 polyunsaturated fatty acid (PUFA) on lipid peroxidation in rats, the formation of malondialdehyde (MDA) and membranes of liver and brain and activities of antioxidant-related enzymes such as catalase, glutathione peroxidase, and superoxide dismutase (SOD) in blood, were studied. Malondialdehyde contents of $\omega3$ PUFA and sardine oil groups were significantly decreased compared with lard group as control (p<0.05). Catalase and superoxide dismutase showed higher activities in $\omega3$ PUFA and sardine oil groups than those of lard control group. These findings suggest that fish oil has a inhibitory effect on formation of lipid peroxides in blood and membranes of rats.
This study was designed to investigate the effects of silk fibroin(Mw 500) powder (SFP) on oxygen radicals and the scavenger enzymes in brain membranes of rats. Spragu-Dawley(SD) male rats(160${\pm}$10g) were fed basic diet(control group), and experimental diets(SFP-2.5 and SFP-5.0 groups) added 2.5 and 5.0g/kg BW/day for 6 weeks. Hydroxyl radical($.$OH) levels resulted in a decreases(6.6% and 9.7%, 2.8% and 11.9%, respectively) in brain mitochondria and microsomes of SFP-2.5 and SFP-5.0 groups compared with control group, but were significantly decreased in these membrances of SFP-5.0 group only. Superoxide radical (O2) levels were a slightly decreased (2.0% and 9.1%, respectively) in brain cytosol of SFP-2.5 and SFP-5.0 groups compared with control group. Lipid peroxide(LPO) levels were significantly decreased (12.9% and 21.9%, 13.2% and 22.5%, respectively) in brain mitochondria and microsomes of SFP-2.5 and SFP-5.0 groups compared with control group. Oxidized protein (OP) levels were significantly decreased (16.7% and 15.7%, respectively) in brain microsomes of SFP-2.5 and SFP-5.0 group compared with control group, but significantly difference between in brain mitochondria of these two groups could not be obtained. Mn-SOD activities were remarkably increased (11.2% and 24.2%, respectively) in mitochodria of SFP-2.5 and SFP-5.0 groups. CuZn-SOD activities were effectively increased (7.7% and 19.6%, respectively) in brain cytosol of SFP-2.5 and SFP-5.0 groups, but significant difference between control and SFP-2.5 groups could be not obtained. GSHPx activities were considerably increased (5.3% and 11.7%, respectively) in brain cytosol of SFP-2.0 and SFP-5.0 groups compared with control group. There results suggest that anti-aging effect of silk fibroin may play an effective learning and memory role in a attenuating a oxidative stress and increasing a scavenger enzyme activity in brain membranes.
KIM JEONG-HWAN;KIM SEUNG-WOOK;YUN CHEOL-WON;CHANG HYO-IHL
Journal of Microbiology and Biotechnology
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v.15
no.3
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pp.633-639
/
2005
Frequently used for humans as a nonsteroidal anti-inflammatory drug, naproxen has been known to induce ulcerative gastric lesions. The present study was undertaken to investigate the in vivo therapeutic effect of astaxanthin, isolated from a Xanthophyllomyces dendrorhous mutant, against naproxen-induced gastric antral ulceration in rats. The rats were treated with three doses of astaxanthin [1, 5, and 25 mg/kg body weight (B.W.), respectively] once daily for 2 weeks after pretreatment of 80 mg of naproxen/kg B.W. twice daily for 3 days, while the control rats received only 80 mg of naproxen/kg B.W. twice daily for 3 days. The oral administration of astaxanthin (1,5, and 25 mg/kg B.W.) showed a curative effect against naproxen (80 mg/kg B.W.)-induced gastric antral ulcer and reduced the elevated lipid peroxide level in gastric mucosa. In addition, astaxanthin treatment resulted in significant increase in the activities of radical scavenging enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. A histologic examination clearly proved that acute gastric mucosal lesion induced by naproxen nearly disappeared after the astaxanthin treatment. These results suggest that astaxanthin eliminated the lipid peroxides and free radicals induced by naproxen and may be a potential candidate for remedy of gastric ulceration.
Objective : The present study was carried out to investigate the preventive effect of Several Herb - Combined Prescription (SHP) on streptozotocin (STZ) - induced diabetes mellitus. Methods : SHP was given to mice with the combination of oral administration and herbal-acupuncture stimulation. Experimental diabetes was induced by the injection of STZ(50mg/kg) to the rat via the peritoneum The effect of SHP on STZ-induced diabetes was observed by measuring the serum level of insulin, glucose, triglyceride, total cholesterol and lipid peroxides. Hepatic activities of catalase and reduced glutathione were examined. Results : SHP treatment protected them from the hyperglycemia. STZ induced increase of serum triglyceride lowered by SHP treatment. Conclusions : The SHP treatment showed protective effect on diabetic mouse model, and action mechanism of the effect was thought to be concerned with anti-oxidative stress.
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