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Objective To investigate the role of heme oxygenase-1(HO-1)in the protective actions of curcumin against ethanol-induced oxidative damage.Methods Microsomal HO-1 enzyme activities were determined in rat primary hepatocytes pretreated by curcumin.AST,LDH release and hepatic oxidative/antioxidant status were measured with or without ZnPPⅨ/Hemin as a classic HO-1 inhibitor/inducer,respectively.Results Curcumin could induce the HO-1 expression and enzyme activity,which was correlated with antioxidant levels in hepatocytes.HO-1 induction reached a peak under administration of 15 μmol/L curcumin for 1 h.Conclusion HO-1 induction by curcumin is contributed to the heptoprotective effects against ethanol-induced oxidative damage.
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In order to study the effect of excessive iodine on immune function of lymphocytes and the role of selenium supplementation with excessive iodine intake, the changes of T lymphocyte number, ratio of subsets, activity of natural killer (NK) cells and lymphocytes proliferation response were investigated. 150 female BALB/C mice were randomly divided into 5 groups in terms of their body weight (n=30 in each group), and 10 of each group were taken as one batch for test. Mice in the 5 groups were orally administrated with iodine 0 (group Ⅰ ), 1500 (group Ⅱ), 3000 (group Ⅲ),6000 μg/L (group Ⅳ), iodine 6000 μg/L plus selenium 0.3 mg/L (group Ⅴ) respectively for 30 days.Lymphocyte proliferation response, CD4+/CD8+, Th1/Th2 and the activity of NK cells were measured. CD4+/CD8+ was significantly lower, while lymphocyte proliferation response stronger, and Th1/Th2 and the activity of NK cells significantly higher in group Ⅳ than in group Ⅰ (P＜0.01).There was no significant difference in all indexes between group Ⅴ and group Ⅰ (P＞0.05). It was suggested that excessive iodine as exogenous chemical materials can induce disorders of T lymphocyte immune function in mice. 0.3 mg/L selenium supplementation can protect mice against toxicity induced by 6000 μg/L iodine.
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Summary: The interaction of high-fat diet and the peptide YY (PYY) gene expression in diet-induced obesity and the mechanisms which predisposed some individuals to become obese on high-fat diet were explored. Thirty-six male SD rats were randomly divided into high-fat diet group (n=27) and chow fed control group (n=9). After 15 weeks of either a high-fat diet or chew fed diet, the high-fat diet group was subdivided into dietary induced obesity (DIO) and dietary induced obesity resistant (DIR) group according to the final body weight. Then the DIO rats were subdivided into two groups for a 8-week secondary dietary intervention. One of the group was switched to chew fed diet, whereas the other DIO and DIR rats continued on the initial high-fat diet. Weight gain and food intake were measured, food efficiency was calculated, and the concentrations of plasma neuropeptide Y (NPY) and PYY were assayed. Hypothalamic NPY mRNA expression and PYY mRNA expression in ileum and colon was detected by RT-PCR. The results showed that at the end of 15th week, the levels of body weight and caloric intake were significantly higher in DIO group than in DIR or control group (P<0.01), while no significant difference was found between DIR and control group (P>0.05). The concentration of plasma PYY was significantly higher in DIR group than in DIO and CF group, while no significant difference was found between DIO and CF group (P<0.01). After switching the DIO rats to chow fed diet, their body weight gains were significantly lower than that of the DIO-HF group. The expression of PYY mRNA was increased in DIO-HF/CF rats than in DIO-HF rats, and the expression of hypothalamic NPY mRNA was decreased in DIO-HF/CF rats than in DIO-HF group. It was concluded that both dietary composition and PYY gene expression could potently alter the hypothalamic NPY expression and result in different susceptibility to obese and overeating. The decreased PYY was associated with the increased NPY expression and their predisposal to obese and overeating in rats.
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Objective: To detect the damage of excessive iodine on the activities and mRNA of cathepsin B and D and observe the effects of selenium intervention. Method: Thyroid follicular epithelial cell line FRTL was cultured in Kaighn’s modified Ham’s F-12 medium. ① The cells were divided into 8 groups for detection of activities of cathepsin B and D (CB and CD). The medium of NI group did not contain selenium or iodine, while EI group contained 50 mmol/L KI, and IS group contained 50mmol/L KI and different dosages of 0.1,0.2,0.5,1.0,2.0 and 5.0 ?mol/L selenium (sodium selenite). ②The mRNA levels of cathepsin B and D were detected by real-time PCR. The medium of NI group and EI group was same as above, but IS group only contained 0.1?mol/L selenium besides 50mmol/L KI. Results: The activities of CB decreased in EI group (50mmol/L KI treated 12 h), while CD decreased after 24 h and both activities were improved in IS groups with 0.1~0.5?mol/L selenium. The mRNA levels of CB and CD in EI group decreased, while in IS group were improved. Conclusion: Excessive iodine resulted in goiter through decreased levels of activities and mRNA of CB and CD. The intervention of selenium on goiter mayinduce its amelioration effect on decrease of CB and CD activities and the optimal dosage ranges from 0.1?mol/L to 0.5?mol/L.
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Objective: To explore the effect of iodine overdose on cathepsin B and D in thyroidcell line (FRTL). Method: The cells were treated with potassium iodide (0, 1, 5, 10, 50 and 100mmol/L). After treatment 6, 12, 24, 48 and 72 hours, the cells were collected. The activities of cathepsin B (CB) and cathepsin D (CD) were assayed by fluorospectrophotometry and Lowry, respectively. The mRNA levels of CB and CD were determined with real-time PCR. Results: After 12 and 24 hours, the activities of CB and CD, treated by 50mmol/L potassium iodide were decreased significanty. The mRNA levels of CB and CD of 50mmol/L potassium iodide group were decreased significanty after treatment 24 hours. Conclusion: The decreased activities of CB and CD were one of reasons of thyroid colloid retention resulted from iodine excess.
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0.2); whereas that in group Ⅲ 1.24 ?0.38g, significantly different (P0.05),the dietary energy re-striction did not affect the producing and scavenging of free radical in theorgans.