ABSTRACT
Glycation and production of free radicals become important mechanisms underlying skin aging. Muntingia calaburais reported to have antioxidant activity in many studies. The effects of M. calabura aqueous leaves extract (MCALE)on oxidative stress and histological changes of mouse model of skin aging were evaluated in this research. Twentymale albino mice were divided into five groups: healthy control; aging control; aging + MCALE 35 mg/kg; aging +MCALE 70 mg/kg; and aging+vitamin C 28 mg/kg. To induce aging condition, oral gavage of D-galactose 500 mg/kg/day were given for 6 weeks. Prior to treatment, blood samples were taken for malondealdehyde (MDA) analyses.MCALE and vitamin C were administered subsequently by oral gavage for 4 weeks and at the end, MDA analyseswere performed again. Routine and van Gieson’s staining were performed to analyze epidermal thickness, fibroblastcell, and density of dermal collagen. Groups received MCALE 70 mg/kg and vitamin C had lower plasma MDAlevel; higher fibroblast number and density of collagen bundles which is reduced in the aging group (p < 0.05).However, epidermal thickness among the five groups was not significantly different. It was concluded that MCALEhad antioxidant and anti-aging effects on D-galactose-induced mouse model of skin aging
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Objective: To investigate the central oxidative stress characteristics of rats with postoperative fatigue syndrome (POFS) and the antifatigue mechanism of ginsenosides Rb1. Methods: Rat models of POFS were established by using the 70% middle part of small bowel resection method. Ninety-six SD rats were randomly divided into control, model, and ginsenoside Rb1 (GRb1, 10 mg/kg) groups by weight. Rats in each group were administered 1 h before operation and were then divided into four subgroups at days 1, 3, 7, and 10. Morris water-maze test was done on postoperative days 2-7. Meanwhile, grasping test, malondialdehyde (MDA) content, superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities were detected on postperative days 1, 3, 7, and 10 and the ultrastructure of hippocampal CA1 area was observed through electron microscope. Results: Compared with the control group, the maximum grip of model rats had an obvious decline on days 3, 7, and 10 (P < 0.05). The total average escape latency was significantly extended (P < 0.05) and the platform crossing times were significantly reduced (P < 0.05). Compared with the model group, the above indexes of rats in GRb1 group were effectively improved after the intervention (P < 0.05). Compared with the control group, on postoperative days 1 and 3, the MDA content was obviously increased (P < 0.05) and SOD activity was obviously raised (P < 0.05). On postoperative day 7, GSH-Px activity was obviously raised (P < 0.05). After the intervention of GRb1, the MDA content was effectively decreased (P < 0.05), SOD and GSH-Px activities were effectively improved (P < 0.05). Electron microscope showed that the ultrastructure of hippocampal CA1 area of rats in GRb1 group was significantly improved. Conclusion: Surgical stress leads to the state change of central oxidative stress; GRb1 could reduce the damage of oxidative stress by strengthening the activity of central anti-oxidant enzymes, so as to protecte central neurons, which may be one of the mechanisms against POFS.
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Objective To illustrate the relationship between the temporary alteration of renal functions of rats with obstructive jaundice due to ischemia reperfusion injury(RI) and lipid peroxidation and the expression of heat shock protein 70 in rat kidney. Methods Wistar rats were divided into 4 groups of sham operation group(S group), sham operation and renal RI group(SRI group), common bile duct ligation group(J group), common bile duct ligation and renal RI group(JRI group). One week after bile duct ligation, rat bilateral renal arteries were transiently occluded for 10 minutes. The variations of renal function were observed at different time phases after renal reperfusion. Simultaneously, the expression of heat shock protein 70 in kidney was evaluated by immunohistochemistry. Results In JRI group, endogenous creatinine clearance rate(Ccr) decreased progressively along with the prolongation of the duration of reperfusion. In J and JRI groups, the level of malondealdehyde(MDA) in renal tissue increased but superoxide dismutase(SOD) decreased. In JRI group, the expression of heat shock protein 70 reached its peak at the 4th hour after reperfusion and began to decrease at the 12 th hour and became lowest at the 24 th hour. No expression of HSP70 was found in other groups. Conclusion The sensitivity of rat kidneys with obstructive jaundice to ischemia reperfusion injury is significantly elevated. Ischemia reperfusion injury, as well as lipid oxidative stress, may be involved in acute renal failure(ARF) after obstructive jaundice surgery. The expression of heat shock protein 70 is a protective response to RI.
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Objective : Oxygen free radicals has been reported to be the critical cellular mediators of experimental ischemia-reperfusion renal injury. We examined the protective effect of allopurinol (an xanthine oxidase inhibitor) on the renal damage by reperfusion in the ischemic rat kidney. METHODS: To induce renal ischemia, the Sprague-Dawley rats(weight 70-80g) were placed in a sealed 5L jar with 8% O2-92% N2 gas mixture for 3.75 hours to the point of gasping, the first sign of asphyxia. Before returning to their metabolic cage, rats were treated with a single subcutaneous injection of allopurinol 135mg/kg or equal volume of saline as control. RESULTS: Reperfusion after renal ischemia in control rats resulted in significant increase of lipid peroxidation at post-reperfusion 15 minutes, compared to postischemia values without significant change of renal function [renal microsomal malondealdehyde (MDA): 8.5+/-0.92 vs 11.4+/-1.72nmol/mg protein, p0.05]. Allopurinol treatment before reperfusion prevented the reflow induced increase of lipid peroxidation at post-reperfusion 15 minutes compared to saline treated control rats [renal microsomal MDA: 11.4+/-1.71 vs 5.5+/-0.65nmol/mg protein, p<0.01), renal PLA2 activity: 0.82+/-0.05 vs 0.32+/-0.03 pmol/mg protein/min, p<0.01]. Ischemia-reperfusion induced renal tubular damages were prevented in allopurinol treated rats. CONCLUSIONS: Allopurinol treatment before reperfusion of ischemic rats reduced the renal lipid peroxidation and tubular necrosis. The role of oxygen free radicals in ischemia-reperfusion injury was indirectly confirmed.