The purpose of this study was to discuss the effect of simulated HiLo training on RBC Hb and HCT of Rats. Sixty male Sprague-Dawley rats were randomly divided into two groups: control group (Ⅰ) and training group (Ⅱ) (n=10). GroupⅠwas divided into normoxia group (A), living-high for 8h (B), living-high for 12h (C). GroupⅡwas divided into normoxia training (D), training on living-high for 8h (E) and training on living-high for 12h (F). The rats of group D、E and F were introduced to treadmill running on an incline of 0 at 25m/min for 1h. After training, the rats of group B, E, C and F were exposed to hypoxic chamber with 12.5% concentrations of oxygen (equal to altitude of 4000m) for 8h and 12h every day for 4 weeks. The red blood cell (RBC), hemoglobin (Hb) and haematocrit (HCT) were determined. The result showed that the increase of RBC Hb and HCT in group B and C were significant. The reduction of RBC, Hb and HCT in group D and E were significant. Comparison between group B and E was significant. It concluded that the simulated hypoxia could increase the level of RBC Hb and HCT, while the simulated HiLo Training could decrease the level of RBC Hb and HCT. The comparisons among the living-high for 8h and living-high for 12h, and training living-high for 8h and training living-high for 12h were not significant.
Previous research demonstrated that diabetes is one of the leading causes of learning and memory deficits. Naringin, a bioflavonoid isolated from grapefruits and oranges, has potent protective effects on streptozotocin (STZ)-induced diabetic rats. Recently, the effects of naringin on learning and memory performances were monitored in many animal models of cognitive impairment. However, to date, no studies have investigated the ameliorative effects of naringin on diabetes-associated cognitive decline (DACD). In this study, we investigated the effects of naringin, using a STZ-injected rat model and explored its potential mechanism.Diabetic rats were treated with naringin (100 mg/kg/d) for 7 days. The learning and memory function were assessed by Morris water maze test. The oxidative stress indicators [superoxide dismutase (SOD) and malondialdehyde (MDA)] and inflammatory cytokines (TNF-a, IL-1β, and IL-6) were measured in hippocampus using corresponding commercial kits. The mRNA and protein levels of PPARγ were evaluated by real time (RT)-PCR and Western blot analysis.The results showed that supplementation of naringin improved learning and memory performances compared with the STZ group. Moreover, naringin supplement dramatically increased SOD levels, reduced MDA levels, and alleviated TNF-α, IL-1β, and IL-6 compared with the STZ group in the hippocampus. The pretreatment with naringin also significantly increased PPARγ expression.Our results showed that naringin may be a promising therapeutic agent for improving cognitive decline in DACD.
Objective To investigate the effects of L-arginine (L-Arg) and aminoguanidine on ischemia-reperfusion injury following rat lung transplantation. Methods The models of rats lung transplantation were established and 4 groups ( n = 6 each) were randomly set up: group A ( normal control group)and treated groups B, C and D. In these groups, different medicines (NS, group A; L-Arg, group B;aminoguanidine, group C; L-Arg and aminoguanidine, group D) were intraperitoneally administered to the recipient rats before reperfusion. After reperfusion for 2 h, the lung graft was harvested for measurements of lung wet/dry ratio ( W/D ) , myeloperoxidase ( MPO ) , malondialdehyde ( MDA ) , superoxide dismutase (SOD) , endothelial nitric oxide synthase (eNOS) , inducible nitric oxide synthase (iNOS). The contents of plasma nitric oxide (NO) were determined. The pathological changes in the lung grafts were observed.Results After reperfusion for 2 h, W/D (5. 10 ±0.21), MPO (1.74 ±0.26) U/g, MDA (20.87 ±2. 90) μmol/g in group B were significantly lower [W/D (5. 74 ± 0. 14), MPO (2. 36 ± 0. 32) U/g,MDA (31. 33 ±3.46) μmol/g] (P ＜ 0. 05), and the levels of SOD (424. 29 ± 27. 86) U/mg protein,NO (175. 12 ± 17. 40) μmol/L, iNOS (3. 62 ±0. 26) U/mg protein and eNOS (5. 36 ±0. 28) U/mg protein were significantly higher than in group A [SOD (268.01 ±26.06) U/mg protein, NO (98.29 ±6.95) μmol/L, iNOS (2.53 ±0.22) U/mg protein and eNOS (3. 57 ±0.40) U/mg protein] (P＜0. 05). The contents of NO (84. 13 ±5. 18) μmol/L and iNOS (1. 81 ±0. 09) U/mg protein in group C were significantly lower than in group A (P ＜ 0. 05). W/D (4. 79 ± 0. 19) , MPO (1. 24 ± 0. 13 ) U/g,MDA (14. 60 ±4. 14) μmol/g, iNOS (1. 99 ±0. 17) U/mg protein were significantly lower than in group A (P ＜0. 05) , and SOD (493. 75 ±24. 95) , NO (149. 61 ± 10. 70) μmol/L and eNOS (5. 50 ±0. 27)U/mg protein in group D were significantly higher than in group A (P＜0. 05). W/D, MPO, MDA, NO and iNOS in group D were significantly reduced as compared with group B (P ＜ 0. 05 ) , and SOD was significantly increased in group B ( P ＜ 0. 05 ) . The pathological examination revealed that the inflammatory cell infiltration in group D was the mildest, followed by groups B, A and C. Conclusion The L-Arg could alleviate the lung ischemia-reperfusion injury after transplantation, the combined used of L-Arg and aminoguanidine could obtain better effects than L-Arg used alone. The aminoguanidine used alone could not alleviate ischemia-reperfusion injury after transplantation.
Key words:
Lung transplantation; Reperfusion injury; Nitric oxide synthase; Arginine; Aminoguanidine
Purpose: To determine the effect of ursolic acid (UA) on diabetes-induced cognitive defect, as well as its mechanism of action in streptozotocin (STZ)-induced diabetic rats.
Methods: A rat model of diabetes was established by administration of STZ. The rats received UA via gastric perfusion for 56 successive days. Learning and memory functions were assessed using Morris water maze. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels in hippocampus tissues were determined spectrophotometrically. Tumor necrosis factor-a (TNF-a), interleukin-1β (IL-1β) and interleukin-6 (IL-6) levels were assayed by quantitative real-time polymerase chain reaction (qRT- PCR) and enzyme-linked immunosorbent assay (ELISA). The protein expression levels of nuclear factor erythroid-2-related factor-2 (Nrf-2), heme oxygenase-1 (HO-1), Bcl-2 and Bax were evaluated by western blotting.
Results: Learning and memory impairment in STZ-induced diabetic rats was mitigated by UA (p < 0.05). In hippocampus tissue, UA reduced oxidative stress by enhancing SOD activity and reducing MDA levels. Furthermore, UA reduced inflammatory response by downregulating TNF-α, IL-1β and IL-6 levels (p < 0.05). Concomitantly, the lower protein concentrations of Nrf-2 and HO-1 were elevated by administration of UA. Furthermore, UA suppressed Bax/Bcl-2 ratio to ameliorate apoptosis (p < 0.05).
Conclusion: UA reduces diabetes-induced hippocampal oxidative stress, inflammation and apoptosis. Thus, it might be a potential drug candidate for delaying diabetes-associated cognitive decline (DACD).
Aging is becoming a prominent health problem in present world. Asiatic acid has multiple health-protecting effects because of its variety biological function. However, relation between asiatic acid and aging is still unknown. In this study, fruit fly was used as model animal to illuminate anti-aging effect of asiatic acid. Our results advised asiatic acid possessed efficacy of promoting health span, as represented by extending lifetime and enhancing locomotor activity both in intrinsic and pathologically aging. In external environment, asiatic acid elevated survival rate against oxidative response and starvation resistance. In aspect of anti-aging mechanism, asiatic acid possessed antioxidant capacity by improvement of super oxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-px) activities and suppression of malondialdehyde (MDA) level to promote health span. In addition, asiatic acid amended energy material storage to meet needs of life process. Moreover, asiatic acid inhibited acetylcholine (AChE) activity to alter cholinergic system in aging process. Lastly, asiatic acid upregulated peroxisome proliferator-activated receptor gamma coactivator 1 (PGC1) and silence information regulator 2 (Sir2) expression in intrinsic aging. In conclusion, asiatic acid exerted health-protecting potential via modulating directly or indirectly antioxidant activity, cholinergic system and longevity genes and could be developed into anti-aging agent.
Grape seed proanthocyanidin extract (GSPE) has been extensively reported to possess a wide range of beneficial properties in multiple tissue damage. Previous studies have shown that exhaustive exercise-induced fatigue associates with oxidative stress injury, inflammatory response, and mitochondrial dysfunction.The aim of this study is to investigate the anti-fatigue effects of GSPE in mice and explore its possible underlying mechanism.The mouse model of exhaustive exercise-induced fatigue was established by using the forced swimming test, and GSPE was orally treated for successive 28 days at 0, 1, 50 and 100 mg/kg/day of body weight, designated the control, GSPE-L, GSPE-M and GSPE-H groups, respectively.The presented results showed that treatment of GSPE at a dose of 50 and 100 mg/kg/day of body weight significantly relieved exhaustive exercise-induced fatigue, indicated by increasing the forced swimming time. In addition, treatment of GSPE significantly improved the creatine phosphokinase and lactic dehydrogenase, as well as lactic acid level in exhaustive swimming. For underlying mechanisms, treatment of GSPE had anti-fatigue effects by promoting antioxidant ability and resisting oxidative effect, as represented by increased total antioxidative capability levels, enhanced superoxide dismutase and catalase activities, and ameliorated malondialdehyde levels. Furthermore, treatment of GSPE significantly inhibited the activity of tumor necrosis factor-α and interleukin-1β, which suggested that its protective effects on exhaustive exercise-induced fatigue may be attributed to inhibition of inflammatory response. Last but not the least, treatment of GSPE significantly improved succinate dehydrogenase and Na+-K+-ATPase levels to enhance mitochondrial function during exhaustive swimming-induced fatigue.These results proved that treatment of GSPE possessed the beneficial properties of anti-inflammatory, antioxidant, and mitochondrial protection to improve exhaustive exercise, which suggested that GSPE could be used as an effective functional food to delay fatigue.
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