Abstract Neurodegenerative diseases include Alzheimer′s disease, Parkinson′s disease, Huntington′s disease, amyotrophic lateral sclerosis, and other disease. There are many causes of neurodegenerative diseases, and the pathogenesis is not entirely clear. Currently, most scholars believe that the occurrence of diseases is closely related to mitochondria. Mitochondrial quality control includes the production, fusion, division, and clearance of mitochondria. Abnormal mitochondrial quality control affects the function of neurons and nerve fibers, leading to the occurrence of neurodegenerative diseases. The author elaborates on the relationship between mitochondria and the pathogenesis of neurodegenerative diseases, providing a basis for the treatment of neurodegenerative diseases.

Objective: To investigate the effect of combined hypoxia and high fat diet (HFD) on endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) of myocardium in experimental rats with its possible mechanisms.
Methods: A total of 60 male SD rats were randomly divided into 3 groups, n=20 in each group. Control group, the rats were fed by normal diet with normal oxygen condition. Hypoxia group, the rats were fed by normal diet with simulated 5000m altitude oxygen condition. Combined hypoxia and HFD (H+HFD) group, the rats were fed by HFD and simulated 5000m altitude oxygen condition. All animals were treated for 4 weeks and peripheral blood and myocardium specimen were collected. Hemoglobin was examined by automatic blood cell analyzer, plasma malondialdehyde (MDA) was measured by TBA method, superoxide dismutase (SOD) activity was detected by WST-1 method, mRNA and protein expressions of eNOS were examined by real time PCR and Western blot analysis respectively, the myocardium nitrates and nitrites (NOx) was measured by nitrate reductase method.
Results: Compared with Control group, Hypoxia group and H+HFD group had increased mRNA and protein expressions of eNOS, H+HFD group had lower NOx levels than the other 2 groups P<0.05. Compared with Hypoxia group, H+HFD group showed obviously increased total cholesterol, LDL-cholesterol and decreased SOD activity, diseased MDA level P<0.05.
Conclusion: Upon hypoxia alone, H+HFD may further reduce NOx level of myocardium, it implies aggravated chronic hypoxia impairment, which might be related to dyslipidemia and lack of anti-oxidative ability in experimental rats.

Objective To investigate the change of aquaporin 2 (AQP2) mRNA and protein levels in renal collecting duct of SD rats after hypoxin caused by rising of the altitude to 4600 m. Methods Forty male SD rats were randomly divided into 4 groups (24 h, 48 h, 72 h and 1 week group), and 10 rats in Xining city were used as control group. All the 40 SD rats were transported to Kekexili Natural Reservation areas (4600 m) in Qinghai province. Rats of four experimental groups were sacrificed and renal tissue samples were harvested at different time point respectively, the control group rats were treated in Xining city (2260 m) as well. The concentration of plasma antidiuretic hormone (ADH) was measured by radioimmunity method. The expression of AQP2 mRNA and proteins was evaluated by real-time fluorescent quantitative-PCR, Western blot and immunofluorescence assay. Results The concentration of plasma ADH was decreased at 24 h and was only 28.5% of that of control group, reaching the lowest concentration at 48 h [(86.94±6.49) μg/L vs (302.5±310.48) μg/L], then it increased gradually and was similar to the control group at 7 d [(306.46±11.14) μg/L vs (302.53±10.48)μg/L, P＞ 0.05]. There were significant differences of the control group with 24 h, 48 h and 72 h groups, respectively[(302.53± 10.48) μg/L vs (142.46±10.57)μg/L, (86.94±6.49)μg/L, (169.65±11.15) μg/L respectively, P＜0.01]. The change of AQP2 gene expression level was consistent with the change of ADH. It was decreased at the begining when exposure to altitude and it reached its lowest level at 48 h. It was then returned to high level similarly to that of the control group at 7 d (0.09±0.01 vs 0.09± 0.008, P＞0.05 ). There were significant differences of the control group with 24 h, 48 h and 72 h group, respectively (0.09±0.008 vs 0.04±0.005, 0.03±0.002, 0.04±0.003 respectively, P＜0.01 ). Conclusions AQP2 expression in the renal collecting duct of SD rats is altered over the period exposed to altitude. It is decreased in the early hypoxia period, and is increased in later period. This change may be related to the intensity of hypoxia, which is mediated by a potential adaptation mechanisms against hypoxia caused by high altitude.

Objective To study the effect of Tibetan medicine Zuotai on in vivo pharmacokinetics of crocin-1 in rats.Methods After im injection of crocin-1 (5 mg/kg) in control (continuously ig normal saline for 7 d) and expermental (continuously ig Zuotai suspension for 7 d or 21 d) rats,The plasma concentration of crocin-1 was determined by RP-HPLC,and plasma concentration-time data were analyzed by DAS 2.0 software to get the related pharmacokinetic parameters of crocin-1.Results After continuously ig administration of Zuotai [10 mg/(kg?d)] for 7 d and 12 d in experimental rats,the pharmacokinetic parameters of crocin-1 changed significantly.The AUC,Cmax,and MRT were significantly greater in experimental rats than those in control rats,and the CL and Vd were significantly lower than those in control rats,and the AUC of crocin-1 was greater in the 21 d administration group than that in the 7 d administration group.Conclusion The result demonstrates that Tibetan medicine significantly affects the pharmacokinetics of crocin-1 in rats.After administration of Zuotai in rats,the absorption degree of crocin-1 is significantly increased and the clearance rate is significantly decreased.

Aim To explore protective effect of Sanweitanxiang powder on isoproterenol-induced myocardial ischemia in rats, and its possible mechanism. Methods A myocardial ischemia model in rats was established by intraperitoneal injection of isoproterenol (Iso 5 mg?kg-1 once a day ,for 3 days). After ip 24 h, The levels of LDH、CK in serum and NOS、iNOS and NO in the myocardium tissue were measured. The myocardial area suffered from ischemia injury were determined. The changes of myocardial ultrastructure were observed with electron microscope. Results Compared with model group, the levels of LDH、CK and infarction size of myocardium were decreased. The concentrations of NOS, iNOS and NO in myocardium were less than those in the model group. The results of myocardial ultrastructure indicated that the partial mitochondria crista and myofibrils sprase, z band unaltered in Sanweitanxiang powder groups. Conclusion Sanweitanxiang powder has a significant protective effect on isoproterenol-induced myocardial injury in rats. By improving the energy metabolism of myocardium,the structure and function of mitochondria and reducing the NO release.