[Vitamins and Immune System Health].

Keeping the immune system healthy forms an effective way to fight infections. Past experience has shown that, in addition to effective interventions including vaccination, drug therapy, and non-pharmaceutical intervention (NPI), dietary nutrition and mental health are also key factors in maintaining immune system health and combating emerging and sudden outbreaks of infections. As the main dietary nutrients, vitamins are active regulators of the immune response and exert a critical impact on the immunity of the human body. Vitamin deficiency causes increased levels of inflammation and decreased immunity, which usually starts in the oral tissues. Appropriate vitamin supplementation can help the body optimize immune function, enhance oral immunity, and reduce the negative impact of pathogen infection on the human body, which makes it a feasible, effective, and universally applicable anti-infection solution. This review focuses on the immunomodulatory effects of vitamin A, B, C, D, and E and proposes that an omics-based new systemic approach will lead to a breakthrough of the limitations in traditional single-factor single-pathway research and provide the direction for the basic and applied research of vitamin immune regulation and anti-infection in all aspects.

Self-reported health problems related to traditional dietary practices in postpartum women from urban, suburban and rural areas of Hubei province, China: the 'zuò yuèzi'.

BACKGROUND AND OBJECTIVES: We aimed to investigate the prevalence of maternal health problems in the postpartum period and their association with traditional Chinese postpartum diets and behaviours in three selected regions in Hubei province, China. METHODS AND STUDY DESIGN: A cross-sectional study was conducted in urban, suburban and rural areas. A total of 2100 women who had given birth to full-term single infants in the past two years were enrolled. Their postpartum diet, personal behaviours, and health problems were surveyed by trained interviewers. RESULTS: During the puerperium women consumed plentiful eggs, fish, poultry and meats; however, fruit, vegetable and milk consumption were limited. A high prevalence of health problems potentially related to pregnancy and the puerperium were found. At least one such problem was reported by 59.3% of women. The putative postpartum problems were backaches (29.6%), arthralgia or leg clonus (12.7%), breast problems (19.6%), constipation (18.7%), haemorrhoids (11.7%), dizziness or headaches (14.8%), anaemia (10.0%). Multiple logistic regression analysis showed that leafy vegetable intake and frequent recipe change in the puerperium were positively associated with less anal diseases. Bathing or hair washing did not increase the risk of maternal infection as belief would have suggested. However, bathing was a risk factor for backache or arthralgia, and tooth brushing was a risk factor for bleeding gums. Excessive housework was a risk factor for anal diseases and disordered uterine involution. CONCLUSION: Postpartum maternal health problems were prevalent in Hubei province. These were in part associated with postpartum traditional Chinese diets and behaviours.

Ameliorative effects of lutein on non-alcoholic fatty liver disease in rats.

AIM: To investigate the therapeutic effects of lutein against non-alcoholic fatty liver disease (NAFLD) and the related underlying mechanism. METHODS: After 9 d of acclimation to a constant temperature-controlled room (20 °C-22 °C) under 12 h light/dark cycles, male Sprague-Darley rats were randomly divided into two groups and fed a standard commercial diet (n = 8) or a high-fat diet (HFD) (n = 32) for 10 d. Animals receiving HFD were then randomly divided into 4 groups and administered with 0, 12.5, 25, or 50 mg/kg (body weight) per day of lutein for the next 45 d. At the end of the experiment, the perinephric and abdominal adipose tissues of the rats were isolated and weighed. Additionally, serum and liver lipid metabolic condition parameters were measured, and liver function and insulin resistance state indexes were assessed. Liver samples were collected and stained with hematoxylin eosin and Oil Red O, and the expression of the key factors related to insulin signaling and lipid metabolism in the liver were detected using Western blot and real-time polymerase chain reaction analyses. RESULTS: Our data showed that after being fed a high-fat diet for 10 d, the rats showed a significant gain in body weight, energy efficiency, and serum total cholesterol (TC) and triglyceride (TG) levels. Lutein supplementation induced fat loss in rats fed a high-fat diet, without influencing body weight or energy efficiency, and decreased serum TC and hepatic TC and TG levels. Moreover, lutein supplementation decreased hepatic levels of lipid accumulation and glutamic pyruvic transaminase content, and also improved insulin sensitivity. Lutein administration also increased the expression of key factors in hepatic insulin signaling, such as insulin receptor substrate-2, phosphatidylinositol 3-kinase, and glucose transporter-2 at the gene and protein levels. Furthermore, high-dose lutein increased the expression of peroxisome proliferators activated receptor-α and sirtuin 1, which are associated with lipid metabolism and insulin signaling. CONCLUSION: These results demonstrate that lutein has positive effects on NAFLD via the modulation of hepatic lipid accumulation and insulin resistance.

Lutein prevents high fat diet-induced atherosclerosis in ApoE-deficient mice by inhibiting NADPH oxidase and increasing PPAR expression.

Epidemiological and experimental studies provide supportive evidence that lutein, a major carotenoid, may act as a chemopreventive agent against atherosclerosis, although the underlying molecular mechanisms are not well understood. The main aim of this study was to investigate the effects of lutein on the alleviation of atherosclerosis and its molecular mechanisms involved in oxidative stress and lipid metabolism. Male apolipoprotein E knockout mice (n = 55) were fed either a normal chow diet or a high fat diet (HFD) supplemented with or without lutein for 24 weeks. The results showed that a HFD induced atherosclerosis formation, lipid metabolism disorders and oxidative stress, but noticeable improvements were observed in the lutein treated group. Additionally, lutein supplementation reversed the decreased protein expression of aortic heme oxygenase-1 and increased the mRNA and protein expressions of aortic nicotinamide-adenine dinucleotide phosphate oxidase stimulated by a HFD. Furthermore, the decreased mRNA and protein expression levels of hepatic peroxisome proliferator-activated receptor-α, carnitine palmitoyltransferase 1A, acyl CoA oxidase 1, low density lipoprotein receptors and scavenger receptor class B type I observed in mice with atherosclerosis were markedly enhanced after treatment with lutein. Taken together, these data add new evidence supporting the anti-atherogenic properties of lutein and describing its mechanisms of action in atherosclerosis prevention, including oxidative stress and lipid metabolism improvements.

Chronic leucine supplementation increases body weight and insulin sensitivity in rats on high-fat diet likely by promoting insulin signaling in insulin-target tissues.

SCOPE: This study investigated the effect of chronic leucine supplementation on insulin sensitivity and the associated mechanisms in rats on high-fat diet (HFD). METHODS AND RESULTS: Male Sprague-Dawley rats were fed either normal chow diet or HFD supplemented with 0, 1.5, 3.0, and 4.5% leucine for 24 weeks. We found that chronic leucine supplementation increased insulin sensitivity together with increased body weight in rats on HFD, but had no effect on insulin sensitivity in rats on normal chow diet. The increased insulin sensitivity by leucine supplementation was not associated with altered ectopic fat accumulation in liver and muscle, plasma levels of lipids and cytokines, but is associated with reduced oxidative stress and improved insulin signaling. Chronic leucine supplementation did not enhance insulin receptor substract-1 (IRS-1) phosphorylation on serine 302, but elevated basal IRS-1 phosphorylation on tyrosine 632 and improved insulin-stimulated protein kinase B (Akt) and mammalian target of rapamycin (mTOR) phosphorylation in liver, skeletal muscle, and adipose tissue of rats on HFD rats, indicating leucine supplementation prevented HFD-induced insulin resistance in insulin-target tissues. CONCLUSION: Chronic leucine supplementation can increase insulin sensitivity and body weight likely by reducing oxidative stress and improving insulin signaling pathway in rats on HFD.

Supplemental selenium alleviates the toxic effects of excessive iodine on thyroid.

As excessive iodine intake is associated with a decrease of the activities of selenocysteine-containing enzymes, supplemental selenium was hypothesized to alleviate the toxic effects of excessive iodine. In order to verify this hypothesis, Balb/C mice were tested by giving tap water with or without potassium iodate and/or sodium selenite for 16 weeks, and the levels of iodine in urine and thyroid, the hepatic selenium level, the activities of glutathione peroxidase (GSHPx), type 1 deiodinase (D1), and thyroid peroxidase (TPO) were assayed. It had been observed in excessive iodine group that hepatic selenium, the activities of GSHPx, D1, and TPO decreased, while in the groups of 0.2 mg/L, 0.3 mg/L and 0.4 mg/L supplemental selenium, the urinary iodine increased significantly. Compared with the group of excessive iodine intake alone, supplemental selenium groups had higher activities of GSHPx, D1, and TPO. We could draw the conclusion that supplemental selenium could alleviate toxic effect of excessive iodine on thyroid. The optimal dosage of selenium ranges from 0.2 to 0.3 mg/L which can protect against thyroid hormone dysfunction induced by excessive iodine intake.

Green tea polyphenols inhibit plasminogen activator inhibitor-1 expression and secretion in endothelial cells.

Compelling epidemiological evidence suggests that the consumption of green tea is associated with beneficial effects in prevention of cardiovascular diseases. Plasminogen activator inhibitor-1 (PAI-1) is known to play a pivotal role in cardiovascular diseases including arteriosclerosis and hypertension. Increased PAI-1 was found in atherosclerotic lesions, and high PAI-1 plasma levels were associated with coronary heart disease. To determine the effect and molecular mechanism of green tea polyphenols (GTPs) on the regulation of PAI-1 expression in endothelial cells, bovine aortic endothelial cells were incubated with GTPs, and PAI-1 expressions were measured by western blot and enzyme-linked immunosorbent assay, respectively. GTPs significantly reduced PAI-1 expression and secretion in a time-dependent and dose-dependent manner. Inhibition of phosphatidylinositol 3-kinase (PI3K) with wortmannin markedly reversed GTPs repression of PAI-1 expression. In addition, the GTP-induced inhibitory effect was associated with an increased of activation of the protein kinase Akt. These results suggest that GTPs inhibit PAI-1 expression and its release from endothelial cells through the PI3K/Akt pathway, which may contribute to cardiovascular protection.

Green tea polyphenols down-regulate caveolin-1 expression via ERK1/2 and p38MAPK in endothelial cells.

Caveolin-1 (Cav-1), a negative regulator of endothelial nitric oxide synthase (eNOS), influences various aspects of the cardiovascular functions. We had reported that a high-fat diet up-regulated aortic Cav-1 expressions in rats. In this study, we investigated the effects of green tea polyphenols (GTPs) on endothelial Cav-1 expression and phosphorylation in vitro. Bovine aortic endothelial cells (BAECs) were treated with 4 microg/ml GTPs for 0, 4, 8, 12, 16 and 24 h, and with 0, 0.04, 0.4, 4 and 40 microg/ml GTPs for 16 h, respectively. Cav-1 protein and mRNA were detected using Western blot and reverse transcriptase polymerase chain reaction. Cav-1 protein expression was down-regulated after treatment of BAECs with 4 microg/ml GTPs for 12, 16 and 24 h. And decrease in the level of Cav-1 mRNA was observed after GTP treatment for 4 and 8 h. GTPs (0.04-4 microg/ml) down-regulate Cav-1 protein expressions and mRNA levels dose dependently. PD98059, an inhibitor of extracellular signal-regulated kinase 1/2 (ERK1/2), up-regulated Cav-1 expression in BAECs alone and abolished the down-regulation effects of GTPs in BAECs while pretreatment with it. Inhibition of p38 mitogen-activated protein kinase (p38MAPK) with SB203580, which down-regulates Cav-1 expression in BAECs alone, deteriorated the Cav-1 down-regulating effects by GTPs. In addition to the effects on expression of Cav-1, GTP treatment inhibited phosphorylation of Cav-1 [tyrosine 14 (Tyr14)]. These data indicate that GTPs down-regulate gene expression of Cav-1 time- and dose- dependently via activating ERK1/2 and inhibiting p38MAPK signaling.

Effect of excessive iodine on immune function of lymphocytes and intervention with selenium.

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 microg/L (group IV), iodine 6000 microg/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 microg/L iodine.

Ginkgo biloba extract prevents ethanol induced dyslipidemia.

Ginkgo biloba extract (EGB) functions as a natural substantial antioxidant and hypolipidemic. Chronic alcohol abuse leads to sustained dyslipidemia characterized by hyperlipidemia and lipid peroxidation. Thus, the present study investigates the effect of EGB on lipid disorders induced by ethanol in rats. Male Sprague-Dawley rats were fed with ethanol (2.4 g/kg), and pretreated with a daily dose of low or high EGB (48 or 96 mg/kg, respectively). During the experiment, serum was collected on day 30, 60, and 90. Serum lipid profile, including lipid peroxidation, was determined by colorimetric methods. Our data showed that ethanol intake resulted in a time-dependent increase in serum levels of triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and malondialdehyde (MDA), and a decrease of the ratio of high-density lipoprotein cholesterol (HDL-C) against TC. EGB prophylactic medication (48 and 96 mg/kg), especially at the high dose, significantly increased HDL-C content, and normalized the abnormal lipid profile and peroxidation in comparison to ethanol-fed only rats. These results suggest that ethanol results in time-dependent hypercholesterolemia, hypertriglyceridemia and promotes serum lipid peroxidation. EGB pretreatment prevents hyperlipidemia and ameliorates lipid peroxidation induced by ethanol.

Heme oxygenase-1 upregulated by Ginkgo biloba extract: potential protection against ethanol-induced oxidative liver damage.

Oxidative stress plays a pivotal role in the pathogenesis and progression of alcoholic liver disease (ALD) and HO-1 induction is suggested to protect hepatocytes from ethanol hepatotoxicity. Here, we present the data to explore the hepatoprotective effect and underlying mechanism(s) of Ginkgo biloba extract (EGB), a naturally occurring HO-1 inducer, against ethanol-induced oxidative damage. Ethanol-fed (2.4 g/kg) male rats were pretreated by EGB (48 or 96 mg/kg) for 90 days. Liver damage was evaluated by histopathology and serum aminotransferase assay. Hepatic redox parameters were measured by spectrophotometry. Heme oxygenase-1 (HO-1) expression was determined by RT-PCR and flow cytometry on mRNA and protein level, respectively. Our results showed that EGB, especially at high dose, ameliorated ethanol-induced macrovesicular steatosis and parenchymatous degeneration in hepatocytes, and decreased serum aminotransferases level. Furthermore, EGB reduced ethanol-derived glutathione depletion and lipid peroxidation, and inhibited the inactivation of superoxide dismutase, glutathione peroxidase and catalase, although EGB itself had no influence on such parameters. Importantly, EGB induced hepatic microsomal HO-1 on mRNA, protein expression and enzymatic activity, which is paralleled to the EGB-derived hepatoprotective effect. Hence, HO-1 upregulation by EGB may enhance the antioxidative capacity against the ethanol-induced oxidative stress and maintain the cellular redox balance.

[Intervention of selenium on neurogranin expression in filial cerebrum of mice with excess iodine].

OBJECTIVE: To study the effects of excess iodine intake on neurogranin expression in cerebrum of filial mice and the intervention of selenium. METHODS: Sixty BALB/c mice were divided randomly into four groups with different drinking water: control group (tap water, NC), excess iodine group (3000 microg/L I, EL +), supplementing selenium group (200 microg/L Se, Se +) and the excess iodine plus selenium (3000 microg/L + I 200 microg/L Se, EI + Se +) group. The mice were mated at the end of the fourth month. Serum T4 and T3 were determined on postnatal day 14 and 28. The expression level of neurogranin in filial cerebrum was measured by immunohistochemistry and Western blot. RESULTS: Serum T4 level in EI (68.78 +/- 11.10 nmol/ L) + was lower significantly than that in NC (100.85 +/- 11.47 nmol/ L) and EI + Se + (93.15 +/- 12.10 nmol/ L) on postnatal day 14. Western blot analysis showed that the relative level of neurogranin in EI + (0.621 +/- 0.041) was lower than that in NC (0.841 +/- 0.039) and EI + Se + (0.781 +/- 0.029) on postnatal day 14 (P < 0.05). No significant difference in serum T4 and neurogranin level between four groups on postnatal day 28. CONCLUSION: Excess iodine intake might change the expression of neurogranin in filial cerebrum and the selenium supplementation might alleviate it.

Effect of Momordica grosvenori on oxidative stress pathways in renal mitochondria of normal and alloxan-induced diabetic mice. Involvement of heme oxygenase-1.

BACKGROUND: Oxidative stress plays an important role in the pathogenesis of diabetes and diabetic nephropathy. Momordica grosvenori (MG), a traditional medicinal herb used as substitute sugar for obese and diabetes, exhibits anti-oxidative activity in vitro. AIM OF THE STUDY: This study investigated the effect of MG on renal mitochondrial lipid peroxidation, anti-oxidative defense system, and a potent oxidative stress-responsive protein, heme oxygenase-1 (HO-1) of nondiabetic and alloxan-diabetic mice in different stages of diabetes. METHODS: Male Balb/c mice were rendered diabetic by a single intra-peritoneal injection of alloxan (200 mg/kg), while control mice received sham saline injection. Control and diabetic mice were further subdivided according to their treatments: control (saline), low dose MG (150 mg/kg) and high dose MG (300 mg/kg), which were administered immediately after confirmation of hyperglycemia by gavage daily over an 8-week period. Mice were killed by cervical dislocation at 4th and 8th week, respectively, and serum and renal tissues were harvested. Serum glucose, lipid profile and renal function were evaluated; renal homogenate were subjected to determination of malondialdehyde (MDA) and glutathione (GSH) concentration, manganese superoxide dismutase (Mn-SOD), glutathione peroxidase (GSH-Px) and HO-1 activities, together with Mn-SOD and HO-1 mRNA expression; paraffin-embedded renal tissues was used for routine histopathological examination. RESULTS: Short-term diabetes caused hyperglycemia and intensified oxidative stress in renal mitochondrial demonstrated by higher MDA and lower GSH levels than control group, accompanied by increased mRNA expression and activity of HO-1 and Mn-SOD, and augmented GSH-Px activity. Low dose of MG administration ameliorated hyperglycemia, inhibited HO-1 and Mn-SOD mRNA expression and reduced HO-1, Mn-SOD, GSH-Px activities. Diabetic mice did not demonstrate early symptoms of diabetic nephropathy until 8th week, characterized by hyperglycemia, hyperlipidemia, and renal damage. A progressive increment in MDA level and decrease in GSH level, as well as reduced mRNA expression and activity of Mn-SOD and HO-1 in the kidney were observed. Low dose of MG attenuated diabetic nephropa- thy symptoms partially, inhibited lipid peroxidation, up-regulated HO-1 and Mn-SOD mRNA expression, and increased HO-1 activity. Conclusions The study confirmed the involvement of oxidative stress in the development of diabetes mediated by the pro- and antioxidant role of HO-1, and pointed to the possible anti-oxidative mechanism of the anti-diabetic and nephroprotective action of MG.

Effect of selenium on thyroid hormone metabolism in filial cerebrum of mice with excessive iodine exposure.

The effects of supplementing selenium on thyroid hormone metabolism were studied on mice with excessive iodine exposure. The serum concentrations of thyroxine (T4) and triiodothyronine (T3) and the activities of iodothyronine 5\' and 5-deiodinase (D2, D3) were measured in the brain of filial mice to study the influence of selenium on thyroid hormone metabolism. Measurements were carried out on postnatal day 0, 14, and 28. It was found that selenium supplementation alleviated the adverse effects of excessive iodine on progeny. The serum TT4 level as well as TT4 and TT3 concentrations and D3 activity in cerebrum of progeny decreased, whereas D2 activity increased in the cerebrum of progeny on postnatal day 0 and 14. Selenium supplementation exerted some favorable effects on thyroid hormone metabolism in cerebrum of progeny of dam with excessive iodine intake.

Effect of selenium supplementation on activity and mRNA expression of type 1 deiodinase in mice with excessive iodine intake.

OBJECTIVE: To investigate the effect of selenium supplementation on the selenium status and selenoenzyme, especially the activity and mRNA expression of type 1 deiodinase (D1) in mice with excessive iodine (EI) intake and to explore the mechanism of selenium intervention on iodine-induced abnormities. METHODS: Weanling female BALB/c mice were given tap water or 3 mg/L of iodine or supplemented with 0.5 mg/L or 1.0 mg/L of selenium in the presence of excessive iodine for 5 months. Selenium status, thyroid hormone level, hepatic and renal D1 activity and mRNA expression were examined. RESULTS: Excessive iodine intake significantly decreased the selenium concentration in urine and liver, and the activity of glutathione peroxidase (GSH-Px) in liver. Meanwhile, serum total T4 (TT4) increased while serum total T3 (TT3) decreased. Hepatic D1 enzyme activity and mRNA expression were reduced by 33% and 86%, respectively. Renal D1 enzyme activity and mRNA were reduced by 30% and 55%, respectively. Selenium supplementation obviously increased selenium concentration, activity of GSH-Px and Dl as well as mRNA expression of D1. However, increasing the supplementation of Se from 0.5 to 1.0 mg/L did not further increase selenoenzyme activity and expression. CONCLUSION: Relative selenium deficiency caused by excessive iodine plays an essential role in the mechanism of iodine-induced abnormalities. An appropriate dose of selenium supplementation exercises a beneficial intervention.

Selenium supplement alleviated the toxic effects of excessive iodine in mice.

The relationship between the iodine intake level of a population and the occurrence of thyroid diseases is U-shaped. When excessive iodine is ingested, hypothyroidism or hyperthyroidism associated with goiter might develop. The aim of the study was to evaluate the effect of Se supplementation on the depression of type 1 deiodinase (D1) and glutathione peroxidase (GSHPx) activities caused by excessive iodine. D1 activity was assayed by the method with 125I-rT3 as a substrate. Compared to the effect of iodine alone, iodine in combination with selenium increased the activities of D1 and GSHPx. The addition of selenium alleviated the toxic effects of iodine excess on the activities of D1 and GSHPx.

[Effect of selenium supplement on the disordered lipid metabolism induced by the overdose of iodine in mice].

OBJECTIVE: To explore the effect of selenium supplement on the disordered lipid metabolism induced by the overdose of iodine in mice. METHODS: The 80 Balb/c mice were randomly divided into eight groups, the normal control group, the high iodine group (drunk the water containing iodine 3000 microg/L) and six selenium groups (drunk the water containing iodine 3000 microg/L and selenium 0.1, 0.2, 0.3, 0.4, 0.5, 0.75 mg/L). The total cholesterol and triglyceride in serum and liver were determined. RESULTS: The total cholesterol in serum, the total cholesterol and triglyceride in liver of high-iodine group increased significantly compared with normal control group. There is no difference between normal control group and the group drunk the water contained 0.2 mg/L selenium. CONCLUSION: It suggests that it is an effective intervention dosage to drunk water containing 0.2 mg/L selenium.

A natural sweetener, Momordica grosvenori, attenuates the imbalance of cellular immune functions in alloxan-induced diabetic mice.

Momordica grosvenori (MG), a traditional medicinal herb in China used as a substitute sugar for obese and diabetic patients, exhibited an enhancement of immunity. Heme oxygenase-1 (HO-1) is among the acute phase proteins that play an important role in the inflammatory process and have antiinflammatory activities with their antioxidant properties. The hypothesis that MG could modulate an imbalance of the cellular immune system and prevent the progression of diabetes mellitus, via induction of HO-1 protein expression was investigated. Diabetes was induced in male Balb/c mice by intraperitoneal injection of alloxan (200 mg/kg). The mice were randomly assigned to non-diabetic and diabetic groups, and further subdivided according to their treatments: control (distilled water), low dose MG (150 mg/kg) and high dose MG (300 mg/kg), which were administered by gavage in 24 h cycles over a 30 day period. MG administration effectively regulated the immune imbalance in diabetic mice, principally by upregulating the CD4(+) T lymphocyte subsets, and remodeling the intracellular cytokine profiles (reducing the expression of pro-inflammatory Th1 cytokines towards a beneficial Th2 pattern), ascribed to its induction and upregulation of HO-1. In conclusion, MG exhibited antidiabetic effects and may be used as a new natural drug for the treatment of diabetes.

[Effect of high-iodine intake on MBP mRNA expression in cerebrum of filial mice and selenium intervention].

OBJECTIVE: To study the effect of selenium supplementation on myelin basic protein (MBP) mRNA expression in cerebrum of high-iodine intake filial mice. METHODS: 135 weanling female Balb/C mice were assigned into 3 groups and given drinking water including different doses of iodine and selenium. Normal control (NC, tap water), high iodine intake group (HI, 3.0 mg/L I of drinking water), high iodine intake and selenium supplementation group I (HI + Se, 3.0 mg/L I + 0.5 mg/L Se of drinking water). All the male and female mice were mated after 4 months later, related indicators of filial mice on 14 day were determined. RESULTS: In filial mice, compared with NC group, serum TT4 decreased significantly in HI groups, TT3 also decreased, and mRNA expression of MBP in cerebrum was down-regulated 27%. The selenium suppleme ntation groups inhibited the decrease of TT4 and TT3, up regulated the m RNA expression of MBP in cerebrum. CONCLUSION: High-iodine Intake can decrease thyroxine of filial mice, which maybe is the reason for down-regulated m RNA expression of MBP in cerebrum, and selenium can exert some intervention by thyroxine, but need to verify more.

[Effect of flavonoids of ginkgo biloba on anti-oxidizing system of mice after acute alcohol administration].

OBJECTIVE: To investigate the protective effects of flavonoids of ginkgo biloba on anti-oxidizing system damaged by acute alcohol administration. METHODS: Adult male Kunming mice were employed and divided into randomly flavonoid intervention group, normal control and ethanol control group according to body weight. After pretreated with flavonoids of ginkgo biloba (96mg/kg bw), the mice in flavonoid intervention group ingested alcohol (ethanol 4.8g/kg bw) via i.g. and were decapitated after 0.5, 1, 2, 4, 6, 9, and 15 h of ethanol administration. The same treatment was carried out on ethanol control group except that physiological saline was applied instead of flavonoid of ginkgo biloba. Meanwhile, the normal control group was established. RESULTS: The concentration of glutathione (GSH), malondialdehyde (MDA) and the activity of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) in the serum and liver were determined. The experiment displays that the content of GSH and the activities of GSH-Px and SOD decreased rapidly after 1 h of treatment with alcohol and dropped to the lowest level at 4h of treatment. After 6h of treatment, these indexes came to the normal level rapidly. The level of MDA of serum and liver increased rapidly after 1 h of treatment and reached the climax at 4h and 6h respectively. It went back to the normal concentration until 15h and 9 h respectively. On a whole, there were similar curves between flavonoids intervention group and alcohol control group on the indexes. However, to some extent, the supplement of flavonoid of ginkgo biloba can prohibit the rise of MDA level and the decline of GSH-Px, SOD, GSH which were induced by acute alcohol intakes. CONCLUSION: Flavonoid of ginkgo biloba have some protective effects on the damage of anti-oxidizing system of mice induced by acute alcohol adminstration.