Objective To study the protective effect of FGP on liver damage in mice caused by carbon tetrachloride(CCl4).Methods Carbon tetrachloride was used to make the model of chemical liver damage.The mice were randomly divided into 5 groups,10 in each:FGP(10.0 ml/kg)+CCl4,FGP(5.0 ml/kg)+CCl4,FGP(2.5 ml/kg)+CCl4,CCl4(0.12%,10 ml/kg)and the control group.The mice were treated with FGP and CCl4 by gavage and intraperitoneal injection.The biochemical and pathological examinations were conducted to observe the liver damage.Results Compared with CCl4 group,treated with FGP at 5.0 ml/kg could reduce the serum ALT activity significantly,the histopathological findings showed an obvious improvement.Conclusion FGP may have some protective effects on acute live damage caused by CCl4 in the mice.

0.05);The rosettes looping rates of the2.5,5.0,10.0 mL/(kg?Bw)polypeptide groups were 33.3%,34.2%,39.6%higher than the control(injected with NS)(P

Objective:To study the effect of multi-micronutrients supplementation on nutritional status of children. Method:220 students aged 8-12 years were observed for 6 months and 1 year follow-up. A half of them was given the supplements, another half as placebo. Results:In comparison with the placebo, the supplemented children had a higher urine excretion of vitamin B2 and vitamin C after loading; a higher concentration of serum 1.25(OH)2D3, hydroxyproline and hydroxyproline/creatinine ratio in fasting urine, and a higher bone mineral content and bone mass density in mid-ulna. The supplemented children performed significantly better than the placebo in reading speed, learning capacity and arithmetic examinations. After one year there was still significant difference between intervention and control group in hemoglobin content and marginal vitamin A deficiency. Conclusion:The micronutrients supplementation played a notable rule in resulting better nutritional status and learning ability of school children, and intervention would have a long effect on their health and nutritional status.

Objective To provide the toxicity basis for safety evaluation of Polyunsaturated Fatty Acids.Methods Acute toxicity test,micronucleus test of born marrow in mice,Ames test,sperm shape abnormality and thirty-day feeding test in rats were conducted in this study.Results The oral LD50 of Polyunsaturated Fatty Acids in both mice and rats were more than 20.0g/kg.BW,so the Polyunsaturated Fatty Acids was classed as actual non-toxicity.The results of micronucleus test of born marrow in mice,Ames test,sperm shape abnormality and thirty-day feeding test in rats were negative.The thirty-day feeding test in rats demonstrated that it had no obvious toxic effects on routine blood,body weight,and biochemical index.No obvious adverse effects dose of this sample was 6.66g/kg.BW.Conclusion Polyunsaturated Fatty Acids toxicity test results showed no obvious toxicity and was safe for edibility.

Objective To study tea polysaccharides(TP) on glucose metabolism,histopathology,and pancreatic islet ?-cell ultrastructure in diabetic mice.Method The alloxan diabetic mice were randomly divided into 4 groups,and orally given distilled water,TP 0.25,0.50,1.00 g/(kg bw?d).for 5 w,and weighed once every week.In experiment 2 and 4 w,the fasting blood glucose was tested once.The glucose tolerance test was conducted at the end of experiments.Blood serum insulin and liver glycogen were measured.The protein content,hexokinase(HK) and pyruvate kinase(PK) activity of 10% liver homogenate were measured.The histopathology of liver,pancreas,kidney and spleen tissue and the ultra structure of pancreas were observed.Results TP could significantly alleviate the symptoms of diabetic mice.The fasting blood glucose values in three TP groups were significantly decreased(P

Objective: To investigate the effects of tea polysaccharide (TP) on blood glucose and diabetic symptoms in mice. Methods: Alloxan-induced diabetic mice were divided into 4 groups, and administered orally with saline, TP at doses of 1.0, 2.0, 4.0 g/kg body weight, respectively for 4 weeks. Water intake and body weight were recorded daily and weekly respectively.Fasting blood samples were collected for measurement of glucose at the end of 2nd and 4th week.Results: Symptoms of diabetic mice fed TP were improved obviously. Their blood glucose concentration and water intake decreased significantly. On the other hand, their body weight increased obviously. There was positive correlation between blood glucose and water intake, but negative correlation between water intake and body weight. Conclusion: TP can decrease blood glucose concentration and improve diabetic symptoms in mice.

Objective:To explore the pathogenesis of flunarizine-induced parkinsonism from gut-brain axis perspective.Methods:Thirty male C57BL/6 mice were randomly divided into control group and flunarizine group ( n=15). Mice in the control group were given 0.1 mL 50% polyethylene glycol 400+50% saline by gavage once/d for 2 weeks, while mice in the flunarizine group were given 6 mg/mL flunarizine+50% polyethylene glycol 400+50% saline by gavage at a daily dose of 30 mg/kg for 2 weeks. Body mass was recorded 1, 3, 5, 7, 10 and 14 d after drug administration, and motor function was assessed by rotarod test 14 d after drug administration; 16s RNA sequencing was performed in the feces to observe the intestinal flora; intestinal transit function was detected by Evans blue by gavage; and then, the mice were sacrificed and homogenate or frozen sections (brain and intestinal tissues) were prepared; dopamine-ergic neuron expression was detected by Western blotting; RT-qPCR was applied to detect the expressions of inflammatory factors in the substantia nigra, and immunofluorescent staining was used to detect the expressions of ZO-1 and Claudin-5 in the intestinal epithelial tissues. Results:Compared with the control group, the flunarizine group had lower body mass ratio 1, 3, 5, 7, 10 and 14 d after drug administration (ratio to body mass before drug administration). Compared with the control group, the flunarizine group had significantly shortened residence time in rod rotating and lower rotational speed when falling ( P<0.05). Compared with the control group, the flunarizine group had decreased tyrosine hydroxylase protein in the substantia nigra without significant difference ( P>0.05). Compared with the control group, the flunarizine group had significantly increased interleukin-6 and tumor necrosis factor-α in the substantia nigra (1.00±0.00 vs. 2.79±0.83; 1.00±0.00 vs. 3.39±1.37), significantly lower intestinal Evans blue propulsion rate (80.67%±4.51% vs. 50.67%±6.03%), and statistically decreased ZO-1 and Claudin-5 expressions in the colonic epithelial tissues (27.01±1.41 vs. 16.32±2.83; 37.00±2.80 vs. 24.52±2.12, P<0.05). Totally, 576 microorganisms were noted in both control group and flunarizine group, 744 in the control group alone, and 634 in the flunarizine group alone. The intestinal flora β diversity indices in the 2 groups were significantly different based on weighted Unifrac-principle coordinates analysis (PCoA, PCoA1: 39.88%; PCoA2: 30.69%). Compared with the control group, the microbial colony structure of mice in flunarizine group was dominated by phylum thick-walled bacteria and phylum warty microbacteria, and by families Muribaculaceae, Lachnospiraceae and Akkermansiaceae. Compared with the control group, the flunarizine group had significantly decreased relative abundance of Ackermannia spp. and Lactobacillus spp. in the intestinal flora ( P<0.05). Conclusion:Flunarizine may contribute to the pathogenesis of DIP by causing structural disturbances in the intestinal flora and inducing neuroinflammation based on the gut-brain axis.