Effects of Climate, Sun Exposure, and Dietary Intake on Vitamin D Concentrations in Pregnant Women: A Population-Based Study.

BACKGROUND: Vitamin D deficiency (VDD) is a global micronutrient issue that commonly occurs in pregnant women, leading to adverse health outcomes. We examined the role of sunlight-related factors and dietary vitamin D intake on vitamin D concentrations among pregnant women in different climate zones. METHODS: We conducted a nationwide cross-sectional survey in Taiwan between June 2017 and February 2019. The data of 1502 pregnant women were collected, including sociodemographic information and characteristics related to pregnancy, diet, and sun exposure. Serum 25-hydroxyvitamin D concentrations were measured, and VDD was assessed as a concentration of less than 20 ng/mL. Logistic regression analyses were used to explore the factors associated with VDD. Furthermore, the area under the receiver operating characteristic (AUROC) curve was used to analyze the contribution of sunlight-related factors and dietary vitamin D intake to vitamin D status stratified by climate zones. RESULTS: The prevalence of VDD was 30.1% and was the highest in the north. Sufficient intake of red meat (odds ratio (OR): 0.50, 95% confidence interval (CI): 0.32-0.75; p = 0.002), vitamin D and/or calcium supplements (OR: 0.51, 95% CI: 0.39-0.66; p < 0.001), sun exposure (OR: 0.75, 95% CI: 0.57-0.98; p = 0.034), and blood draw during sunny months (OR: 0.59, 95% CI: 0.46-0.77; p < 0.001) were associated with a lower likelihood of VDD. Additionally, in northern Taiwan, which is characterized by a subtropical climate, dietary vitamin D intake (AUROC: 0.580, 95% CI: 0.528-0.633) had a greater influence on vitamin D status than did sunlight-related factors (AUROC: 0.536, 95% CI: 0.508-0.589) with a z value = 51.98, p < 0.001. By contrast, sunlight-related factors (AUROC: 0.659, 95% CI: 0.618-0.700) were more important than dietary vitamin D intake (AUROC: 0.617, 95% CI, 0.575-0.660) among women living in tropical areas of Taiwan (z value = 54.02, p < 0.001). CONCLUSIONS: Dietary vitamin D intake was essential to alleviate VDD in the tropical region, whereas sunlight-related factors played a greater role in subtropical areas. Safe sunlight exposure and adequate dietary vitamin D intake should be promoted appropriately as a strategic healthcare program.

Polymorphisms of haptoglobin modify the relationship between dietary iron and the risk of gestational iron-deficiency anemia.

PURPOSE: To assess whether polymorphisms of haptoglobin (Hp) modify the relationship between dietary iron and the risk of gestational iron-deficiency anemia (IDA). METHODS: This study analyzed 1430 singleton pregnant women aged 20 ~ ≤ 48 years from the 2017-2019 National Nutrition and Health Survey of Pregnant Women in Taiwan. Sociodemographic, blood biochemical, Hp phenotype, and 24-h dietary recall data were collected. Erythropoiesis-related total prenatal supplementation was defined as the reported use of multivitamins and minerals, vitamin B complex, folate, and iron. RESULTS: Distributions of the Hp 1-1, Hp 2-1, and Hp 2-2 phenotypes were 13.6, 39.8, and 46.5%, respectively. Women with the Hp 1-1 phenotype had the lowest mean levels of serum ferritin (p-trend = 0.017), the highest prevalence of gestational ID (p-trend = 0.033) as well as the highest prevalence of gestational IDA (did not reach statistical differences, p-trend = 0.086). A gene-diet interaction on serum ferritin was observed between the Hp 1 and Hp 2 (2-1/2-2) alleles (p < 0.001). An adjusted multivariate logistic regression showed that compared to those with a normal blood iron status and who reported using erythropoiesis-related total prenatal supplements, those who did not had a 4.05-fold [odds ratio (OR) = 4.05 (95% confidence interval (CI) 2.63-6.24), p < 0.001] increased risk of gestational IDA. The corresponding ORs for carriers of the Hp 1 and Hp 2 alleles were 4.78 (95% CI 1.43-15.99) and 3.79 (95% CI 2.37-6.06), respectively. CONCLUSION: Pregnant women who are Hp 1 carriers are at increased risk for developing IDA if they do not meet the recommended dietary allowance for iron or use erythropoiesis-related prenatal supplements.

C-Phycocyanin and Lycium barbarum Polysaccharides Protect against Aspirin-Induced Inflammation and Apoptosis in Gastric RGM-1 Cells.

Aspirin causes gastrotoxicity and damaged epithelial defense via cyclooxygenase inhibition. C-phycocyanin (CPC) and Lycium barbarum polysaccharides (LBP), an active ingredient of Spirulina platensis and wolfberry, respectively, exerted antioxidation, anti-inflammation, and/or immunoregulation. The actions of CPC and/or LBP on gastric damage induced by aspirin were explored in rat gastric mucosal RGM-1 cells. Gastric injury was performed by 21 mM aspirin for 3 h after the pretreatment of CPC and/or LBP (100-500 µg/mL) for 24 h in RGM-1 cells. Proinflammatory, anti-inflammatory, and apoptotic markers were examined by ELISA or gel electrophoresis and Western blotting. Cell viability and interleukin 10 (IL-10) were reduced by aspirin. Increased proinflammatory markers, caspase 3 activity, and Bax protein were observed in RGM-1 cells with aspirin treatment. Aspirin elevated nuclear factor-κB (NF-κB), extracellular signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK) activation, while CPC and/or LBP increased IL-10, and attenuated proinflammatory markers, Bax protein, NF-κB, and the activation of ERK and JNK. Therefore, CPC and/or LBP possess anti-inflammation by restraining the activation of the ERK signaling pathway, and LBP decreases apoptosis by suppressing the JNK signaling pathway activation in gastric RGM-1 cells with aspirin-induced epithelial damage.

Lycium barbarum Polysaccharides and Capsaicin Inhibit Oxidative Stress, Inflammatory Responses, and Pain Signaling in Rats with Dextran Sulfate Sodium-Induced Colitis.

Ulcerative colitis (UC) is an inflammatory disease with chronic relapsing symptoms. This study investigated the effects of Lycium barbarum polysaccharides (LBP) and capsaicin (CAP) in dextran sulfate sodium (DSS)-induced UC rats. Rats were divided into normal, DSS-induced UC, and UC treated with 100 mg LBP/kg bw, 12 mg CAP/kg bw, or 50 mg LBP/kg bw and 6 mg CAP/kg bw. Rats were fed LBP or CAP orally by gavage for 4 weeks, and UC model was established by feeding 5% DSS in drinking water for 6 days during week 3. Oral CAP and mixture significantly reduced disease activity index. Oral LBP significantly decreased serum malondialdehyde, interleukin (IL)-6, colonic tumor necrosis factor (TNF)-α levels, and protein expression of transient receptor potential cation channel V1 (TRPV1) and transient receptor potential ankyrin 1 (TRPA1), but increased serum catalase activity. Oral CAP significantly suppressed serum IL-6, colonic TRPV1 and TRPA1 protein expression, but elevated IL-10 levels, serum superoxide dismutase and catalase activities. The mixture of LBP and CAP significantly reduced serum IL-6, colonic TNF-α and TRPA1 protein. In conclusion, administration of LBP and/or CAP attenuate DSS-induced UC symptoms through inhibiting oxidative stress, proinflammatory cytokines, and protein expression of TRPV1 and TRPA1.

Gut Microbiota as a Mediator of Essential and Toxic Effects of Zinc in the Intestines and Other Tissues.

The objective of the present study was to review the existing data on the association between Zn status and characteristics of gut microbiota in various organisms and the potential role of Zn-induced microbiota in modulating systemic effects. The existing data demonstrate a tight relationship between Zn metabolism and gut microbiota as demonstrated in Zn deficiency, supplementation, and toxicity studies. Generally, Zn was found to be a significant factor for gut bacteria biodiversity. The effects of physiological and nutritional Zn doses also result in improved gut wall integrity, thus contributing to reduced translocation of bacteria and gut microbiome metabolites into the systemic circulation. In contrast, Zn overexposure induced substantial alterations in gut microbiota. In parallel with intestinal effects, systemic effects of Zn-induced gut microbiota modulation may include systemic inflammation and acute pancreatitis, autism spectrum disorder and attention deficit hyperactivity disorder, as well as fetal alcohol syndrome and obesity. In view of both Zn and gut microbiota, as well as their interaction in the regulation of the physiological functions of the host organism, addressing these targets through the use of Zn-enriched probiotics may be considered an effective strategy for health management.

Phytochemistry, Pharmacology, and Nutraceutical Profile of Carissa Species: An Updated Review.

Carissa, a genus of the Apocynaceae family, consists of evergreen species, such as shrubs as well as small trees that are native to Asia, Africa, and Oceania's subtropical and tropical regions. Most of the Carissa species are traditionally used to treat various diseases, such as chest pain, headaches, gonorrhoea, rheumatism, syphilis, oedema, rabies, stomach pain, hepatitis, cardiac diseases, and asthma. The pharmacological studies on Carissa species revealed its antioxidant, antimicrobial, anticancer, cardioprotective, antipyretic, analgesic, wound healing, anticonvulsant, antiarthritic, adaptogenic, anti-inflammatory, and antidiabetic activities, thus validating its use in indigenous medicine systems. The review article summarised the comprehensive literature available, including morphology, indigenous uses, bioactive composition, nutraceutical, and pharmacological activities of Carissa species. A total of 155 research papers were cited in this review article. The Carissa fruits are rich in dietary fibre, lipids, proteins, carbohydrates, vitamin C, and macro- and micro-elements. A total of 121 compounds (35 polyphenols (flavonoids and phenolic acids), 30 lignans, 41 terpenoids, 7 steroids, 2 coumarins, and 6 cardiac glycosides) have been extracted from C. spinarum, C. carandas, and C. macrocarpa. Among all chemical constituents, lupeol, carissol, naringin, carisssone, scopoletin, carissaeduloside A, D, J, carandinol, sarhamnoloside, carissanol, olivil, carinol, 3ß-hydroxyolean-11-en-28,13ß-oilde, ursolic acid, and carissone are the key bioactive constituents responsible for pharmacological activities of genus Carissa. The gathered ethnopharmacological information in the review will help to understand the therapeutic relevance of Carissa as well as paving a way for further exploration in the discovery of novel plant-based drugs.

Selenium, Zinc, Chromium, and Vanadium Levels in Serum, Hair, and Urine Samples of Obese Adults Assessed by Inductively Coupled Plasma Mass Spectrometry.

The objective of this study was to investigate of selenium (Se), zinc (Zn), chromium (Cr), and vanadium (V) levels in blood serum, hair, and urine of adult obese patients. A total of 199 lean and 196 obese subjects were enrolled in the study. Serum, hair, and urinary metal and metalloid analysis were performed by inductively coupled plasma mass spectrometry at NexION 300D (PerkinElmer Inc., USA). The results established that obese subjects were characterized by 47% and 30% lower serum Cr and V levels compared with controls, respectively, whereas serum Se levels exceeded control values by 9%. In contrast, hair Cr, Se, and V content in obese subjects exceeded the control values by 51%, 21%, and 50%, respectively. In turn, hair Zn levels were found to be significantly lower by 11% compared with the lean control values. In urine, the levels of V and Zn were found to be 30% and 18% higher in obese patients. Prevalence of hypertension in obese subjects was associated with a trend for impaired Se and Zn levels. In a regression model adjusted for age, gender, hypertension, atherosclerosis, and glucose intolerance, serum Cr, V, and hair Zn were inversely associated with body mass index (BMI), whereas hair Se was considered as the positive predictor. Our data allow proposing that the observed alterations may at least partially contribute to metabolic disturbances in obesity. In turn, monitoring of Se exposure in a well-nourished adult population is required to reduce its potential contribution to obesity.

Gastroprotective effect of Lycium barbarum polysaccharides and C-phycocyanin in rats with ethanol-induced gastric ulcer.

This study investigated the gastroprotective effect of Lycium barbarum polysaccharides (LBP) and C-phycocyanin (C-PC) in rats with ethanol-induced gastric ulcer. Rats were divided into 5 groups: normal, ulcer, ulcer treated with 100 mg/kg bw LBP, ulcer treated with 50 mg/kg bw C-PC, and ulcer treated with 50 mg/kg bw LBP and 25 mg/kg bw C-PC. Pretreatment with LBP and/or C-PC was given a week before ulcer induction. Ulcer induction was produced by 50% ethanol administration orally every other day for 4 weeks. After 5-week treatment, the histopathological observation showed that LBP or C-PC attenuated the severity of gastric mucosal damage. LBP decreased serum malondialdehyde (MDA) levels and gastric interleukin-6 (IL-6), intercellular adhesion molecule-1 (ICAM-1) levels, and myeloperoxidase (MPO) activity. C-PC decreased serum MDA levels and gastric tumor necrosis factor-α (TNF-α), IL-1ß, IL-6, ICAM-1 levels, and MPO activity. Combined LBP and C-PC decreased serum MDA levels and gastric TNF-α, IL-1ß, IL-6, and ICAM-1 levels. LBP and/or C-PC increased gastric heat shock protein 70 and non-protein sulfhydryl compounds. Rats with ulcer and treatment had enriched with the family Bacillaceae. Therefore, pretreatment with LBP and/or C-PC attenuated ethanol-induced gastric ulcer in rats via suppressing oxidation and inflammation and increasing gastroprotection.

Effects of fish oil and spirulina on oxidative stress and inflammation in hypercholesterolemic hamsters.

BACKGROUND: Altered plasma lipids, oxidative stress, and inflammation have been involved in the pathogenesis of cardiovascular disease. Fish oil has shown inconclusive effects on plasma lipids and oxidative stress. Spirulina has both cholesterol lowering and antioxidant properties. However, the effect of fish oil and spirulina on hypercholesterolemia has not been studied. We investigated the effects of fish oil, spirulina, and their combination on hypercholesterolemia. METHODS: The hamsters were divided into 7 groups: control, high cholesterol (HF), fish oil (post FO), spirulina (post SP), and a combination of fish oil and spirulina (post SF, pre-SF, and HF + SF) groups. The HF and HF + SF groups were given a high cholesterol diet for 8 weeks. The post FO, post SP, and post SF groups were given a high cholesterol diet for 4 weeks and then the treatment for 4 weeks. The pre-SF group was given the combined treatment for 4 weeks and then a high cholesterol diet for 4 weeks. RESULTS: The HF and HF + SF groups altered plasma lipids, increased oxidative stress, inhibited antioxidants, and increased inflammation. While the post FO group increased plasma lipids and was more atherogenic. The vice versa was observed in spirulina-treated group. Both the post SP and post SF groups inhibited oxidative stress and increased antioxidant status, and post FO and post SP diets regulated pro-inflammatory cytokines to near the control levels. CONCLUSIONS: Both single treatment of fish oil or spirulina inhibit oxidative stress and inflammation. Treatment with a combination of fish oil and spirulina (post SF) may be beneficial for diet-induced hypercholesterolemic hamsters.

Ginseng extract and ginsenoside Rb1 attenuate carbon tetrachloride-induced liver fibrosis in rats.

BACKGROUND: Ginsenosides, the major bioactive compounds in ginseng root, have been found to have antioxidant, immunomodulatory and anti-inflammatory activities. This study investigated the effects of ginsenosides on carbon tetrachloride (CCl4)-induced hepatitis and liver fibrosis in rats. METHODS: Male Sprague-Dawley rats were randomly divided into four groups: control, CCl4, CCl4 + 0.5 g/kg Panax ginseng extract and CCl4 + 0.05 g/kg ginsenoside Rb1 groups. The treated groups were orally given Panax ginseng extract or ginsenoside Rb1 two weeks before the induction of liver injury for successive 9 weeks. Liver injury was induced by intraperitoneally injected with 400 ml/l CCl4 at a dose of 0.75 ml/kg body weight weekly for 7 weeks. The control group was intraperitoneally injected with olive oil. RESULTS: The pathological results showed that ginsenoside Rb1 decreased hepatic fat deposition (2.65 ± 0.82 vs 3.50 ± 0.75, p <0.05) and Panax ginseng extract lowered hepatic reticular fiber accumulation (1.05 ± 0.44 vs 1.60 ± 0.39, p <0.01) increased by CCl4. Plasma alanine aminotransferase and aspartate aminotransferase activities were increased by CCl4 (p <0.01), and aspartate aminotransferase activity was decreased by Panax ginseng extract at week 9 (p <0.05). Exposure to CCl4 for 7 weeks, the levels of plasma and hepatic triglycerides (p <0.01), hepatic cholesterol (p <0.01), interleukin-1ß (p <0.01), prostaglandin E2 (p <0.05), soluble intercellular adhesion molecule-1 (p <0.05), hydroxyproline (p <0.05), matrix metalloproteinase-2 (p <0.05) and tissue inhibitor of metalloproteinase-1 (TIMP-1) (p <0.01) were elevated, however, hepatic interleukin-10 level was lowered (p <0.05). Both Panax ginseng extract and ginsenoside Rb1 decreased plasma and hepatic triglyceride, hepatic prostaglandin E2, hydroxyproline and TIMP-1 levels, and Panax ginseng extract further inhibited interleukin-1ß concentrations (p <0.05). CONCLUSIONS: Panax ginseng extract and ginsenoside Rb1 attenuate plasma aminotransferase activities and liver inflammation to inhibit CCl4-induced liver fibrosis through down-regulation of hepatic prostaglandin E2 and TIMP-1.

Beneficial effects of catechin-rich green tea and inulin on the body composition of overweight adults.

Green tea catechin has been proposed to have an anti-obesity effect. The aim of the present study was to investigate whether the effect of catechin-rich green tea in combination with inulin affects body weight and fat mass in obese and overweight adults. A total of thirty subjects were divided into a control group and an experimental group who received 650 ml tea or catechin-rich green tea plus inulin. A reduction of body weight ( - 1·29 (sem 0·35) kg) and fat mass (0·82 (sem 0·27) kg) in the experimental group was found after 6 weeks, and no adverse effects were observed. After refraining from consumption for 2 weeks, sustained effects on body weight and fat mass were observed. We conclude that continuous intake of catechin-rich green tea in combination with inulin for at least 3 weeks may be beneficial for weight management.

Hot water extracted Lycium barbarum and Rehmannia glutinosa inhibit liver inflammation and fibrosis in rats.

Polysaccharide-rich Lycium barbarum and Rehmannia glutinosa have been considered to have immune-modulating activity. This study investigated the effects of water extracted Lycium barbarum and Rehmannia glutinosa (HE) on carbon tetrachloride (CCl(4))-induced liver injury in rats. Male Sprague-Dawley rats were randomly divided into: normal diet + peritoneal injection of olive oil (control), normal diet + CCl(4) injection (CCl(4)), 1 × HE (0.05% HE for each) + CCl(4) (1 × HE), and 3 × HE (0.15% HE for each) + CCl(4) (3 × HE) groups. Rats were injected with 40% CCl(4) at a dose of 0.75 ml/kg body weight once a week for seven weeks, one week after herbal extract treatment. After eight week herbal extract treatment, pathohistological examination showed that both 1× and 3 × HE treatments diminished necrotic hepatocytes, chemoattraction of inflammatory cells, and liver fibrosis. Both 1× and 3 × HE treatments decreased plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, and reduced hepatic levels of pro-inflammatory cytokines - tumor necrosis factor-α and interleukin-1ß - compared to CCl(4) treatment alone. The 1 × HE treatment increased hepatic anti-inflammatory cytokine IL-10 levels. Both the 1× and 3 × HE treatments suppressed liver fibrosis biomarkers - transforming growth factor-ß1 and hydroxyproline. Therefore, treatment with water extracted Lycium barbarum and Rehmannia glutinosa (0.05% and 0.15% for each) for eight weeks protects against necrotic damage, indicated by decreases in plasma ALT and AST activities, and suppresses liver fibrosis by down-regulation of liver inflammation in rats with CCl(4)-induced liver injury.

Ginsenoside Rb1 inhibits cell activation and liver fibrosis in rat hepatic stellate cells.

Chronic hepatitis/cirrhosis is the eighth leading cause of death in Taiwan. Excess accumulated extracellular matrix produced by activated hepatic stellate cells (HSCs) is the major cause of liver fibrosis. Ginsenoside Rb1, the most active compound purified from ginseng, has been considered to be hepatoprotective. This study investigated the effects of ginsenoside Rb1 (98.8% purity) on activation, proliferation, and profibrotic factors in rat HSC-T6 cells under H2O2 oxidative stress. Rat HSC-T6 cells were activated by 10 nM H2O2 and then incubated with different concentrations of ginsenoside Rb1 (5, 10, 20, 40, and 80 µg/mL) for 24 hours. Medium containing 0.08% dimethyl sulfoxide or 5 mM N-acetyl-l-cysteine was used as a negative or positive control, respectively. The results showed that ginsenoside Rb1 at 5-40 µg/mL significantly reduced α-smooth muscle actin levels and at 5-80 µg/mL inhibited cell proliferation in HSC-T6 cells after induction with H2O2 (P<.05). Collagen secreted by HSC-T6 cells was decreased by ginsenoside Rb1 at 5-80 µg/mL (P<.05). Protein expression of transforming growth factor-ß1 (TGF-ß1), matrix metalloproteinase (MMP)-2, and tissue inhibitor of metalloproteinase (TIMP)-1 was suppressed by ginsenoside Rb1 at 10-80 µg/mL (P<.05). In addition, mRNA expression of type I and III collagen, TGF-ß1, and TIMP-1 was inhibited by ginsenoside Rb1 (10 and 80 µg/mL) (P<.05). Therefore, ginsenoside Rb1 exerted an antifibrotic effect on HSCs by inhibiting activation, proliferation, and expression of collagen, TGF-ß1, MMP-2, and TIMP-1.

Curcumin and saikosaponin a inhibit chemical-induced liver inflammation and fibrosis in rats.

Curcumin and saikosaponin A as antioxidants improve antioxidant status. This study investigated the anti-inflammatory and antifibrotic actions of curcumin and saikosaponin A on CCl(4)-induced liver damage. Sprague-Dawley rats were randomly divided into control, CCl(4), CCl(4)+ curcumin (0.005%; CU), CCl(4) + saikosaponin A (0.004%; SS), and CCl(4) + curcumin + saikosaponin A (0.005% + 0.004%; CU + SS) groups. Carbon tetrachloride (40% in olive oil) at a dose of 0.75 ml/kg was injected intraperitoneally once a week. Curcumin and saikosaponin A were supplemented alone or in combination with diet 1 week before CCl(4) injection for 8 weeks. After 8-week supplementation, histopathological results showed hepatic collagen deposition was significantly reduced in the CU and SS groups, and activated nuclear factor-kappa B expression induced by CCl(4) in the liver was significantly inhibited by curcumin and/or saikosaponin A. Hepatic proinflammatory cytokines tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 were significantly inhibited, and anti-inflammatory cytokine interleukin-10 was significantly increased by supplementation with curcumin and/or saikosaponin A. Additionally, curcumin and/or saikosaponin A significantly reduced the increased levels of hepatic transforming growth factor-beta1 and hydroxyproline after CCl(4) treatment. Therefore, supplementation with curcumin and/or saikosaponin A suppress inflammation and fibrogenesis in rats with CCl(4)-induced liver injury. However, the combination has no additive effects on anti-inflammation and antifibrosis.

Curcumin or saikosaponin a improves hepatic antioxidant capacity and protects against CCl4-induced liver injury in rats.

Curcumin and saikosaponin a, the bioactive phytochemicals of turmeric and Bupleurum, act as antioxidants. This study investigated the effects of supplementation with curcumin and/or saikosaponin a on hepatic lipids and antioxidant status in rats with CCl(4)-induced liver injury. Male Sprague-Dawley rats were randomly divided into control, CCl(4), CCl(4) + curcumin (0.005%; CU), CCl(4) + saikosaponin a (0.004%; SS), and CCl(4) + curcumin + saikosaponin a (0.005% + 0.004%; CU+SS) groups. CCl(4) (40% in olive oil) was injected intraperitoneally at a dose of 0.75 mL/kg once a week. Curcumin and/or saikosaponin a was administered orally 1 week before CCl(4) injection for 8 weeks. The pathological results showed that liver fibrosis was ameliorated in the SS and CU+SS groups. After 8 weeks, supplementation with curcumin and/or saikosaponin a significantly decreased plasma alanine aminotransferase and aspartate aminotransferase activities, as well as plasma and hepatic cholesterol and triglyceride levels. The CU+SS group showed reversal of the impaired hepatic superoxide dismutase activity and an increase in total glutathione level. Supplementation with curcumin and/or saikosaponin a significantly improved hepatic antioxidant status and suppressed malondialdehyde formation. Therefore, supplementation with curcumin and/or saikosaponin a protects against CCl(4)-induced liver injury by attenuating hepatic lipids and lipid peroxidation and enhancing antioxidant defense. Curcumin and saikosaponin a had no additive effects on hepatoprotection except for greater improvement in the total glutathione level and antioxidant status.

Protective effects of Ginkgo biloba, Panax ginseng, and Schizandra chinensis extract on liver injury in rats.

This study investigated the effects of the combined extracts of Ginkgo biloba, Panax ginseng, and Schizandra chinensis at different doses on hepatic antioxidant status and fibrosis in rats with carbon tetrachloride (CCl4)-induced liver injury. Male Sprague-Dawley rats (n = 8-12 per group) were divided into the control, CCl4, CCl4 + silymarin (0.35%), CCl4 + low-dose herbal extract (0.24% of Ginkgo biloba, Panax ginseng, and Schizandra chinensis extract at 1:1:1; LE), and CCl4 + high-dose herbal extract (1.20% of the same herbal extract; HE) groups. Silymarin or herbal extract was orally given to rats a week before chronic intraperitoneal injection with CCl4 for 6 weeks. The pathological results showed that herbal extract suppressed hepatic bile duct proliferation, and low-dose herbal extract inhibited liver fibrosis. Hepatic superoxide dismutase (SOD) activity was lower in the CCl4 group, but there was no difference in the silymarin or herbal extract treated groups compared to the control group. Hepatic catalase activity and the ratio of reduced to oxidized glutathione were significantly higher (p < 0.05) in the HE group than those in the CCl4 group. Silymarin and herbal extract reversed the impaired hepatic total antioxidant status (p < 0.05). Herbal extract partially reduced the elevated hepatic lipid peroxides. Hepatic transforming growth factor-beta1 (TGF-beta1) level decreased significantly (p < 0.05) in the LE group. Therefore, high-dose herbal extract improved hepatic antioxidant capacity through enhancing catalase activity and glutathione redox status, whereas low-dose herbal extract inhibited liver fibrosis through decreasing hepatic TGF-beta1 level in rats with CCl4-induced liver injury.

Hot water-extracted Lycium barbarum and Rehmannia glutinosa inhibit proliferation and induce apoptosis of hepatocellular carcinoma cells.

AIM: To investigate the effect of hot water-extracted Lycium barbarum (LBE) and Rehmannia glutinosa (RGE) on cell proliferation and apoptosis in rat and/or human hepatocellular carcinoma (HCC) cells. METHODS: Rat (H-4-II-E) and human HCC (HA22T/VGH) cell lines were incubated with various concentrations (0-10 g/L) of hot water-extracted LBE and RGE. After 6-24 h incubation, cell proliferation (n = 6) was measured by a colorimetric method. The apoptotic cells (n = 6) were detected by flow cytometry. The expression of p53 protein (n = 3) was determined by SDS-PAGE and Western blotting. RESULTS: Crude LBE (2-5 g/L) and RGE (2-10 g/L) dose-dependently inhibited proliferation of H-4-II-E cells by 11% (P < 0.05) to 85% (P < 0.01) after 6-24 h treatment. Crude LBE at a dose of 5 g/L suppressed cell proliferation of H-4-II-E cells more effectively than crude RGE after 6-24 h incubation (P < 0.01). Crude LBE (2-10 g/L) and RGE (2-5 g/L) also dose-dependently inhibited proliferation of HA22T/VGH cells by 14%-43% (P < 0.01) after 24 h. Crude LBE at a dose of 10 g/L inhibited the proliferation of HA22T/VGH cells more effectively than crude RGE (56.8% +/- 1.6% vs 70.3% +/- 3.1% of control, P = 0.0003 < 0.01). The apoptotic cells significantly increased in H-4-II-E cells after 24 h treatment with higher doses of crude LBE (2-5 g/L) and RGE (5-10 g/L) (P < 0.01). The expression of p53 protein in H-4-II-E cells was 119% and 143% of the control group compared with the LBE-treated (2, 5 g/L) groups, and 110% and 132% of the control group compared with the RGE -treated (5, 10 g/L) groups after 24 h. CONCLUSION: Hot water-extracted crude LBE (2-5 g/L) and RGE (5-10 g/L) inhibit proliferation and stimulate p53-mediated apoptosis in HCC cells.

Protective effects of Ginkgo biloba extract on the ethanol-induced gastric ulcer in rats.

AIM: To evaluate the preventive effect of Ginkgo biloba extract (GbE) on ethanol-induced gastric mucosal injuries in rats. METHODS: Female Wistar albino rats were used for the studies. We randomly divided the rats for each study into five subgroups: normal control, experimental control, and three experimental groups. The gastric ulcers were induced by instilling 1 mL 50% ethanol into the stomach. We gave GbE 8.75, 17.5, 26.25 mg/kg intravenously to the experimental groups respectively 30 min prior to the ulcerative challenge. We removed the stomachs 45 min later. The gastric ulcers, gastric mucus and the content of non-protein sulfhydryl groups (NP-SH), malondialdehyde (MDA), c-Jun kinase (JNK) activity in gastric mucosa were evaluated. The amount of gastric juice and its acidity were also measured. RESULTS: The findings of our study are as follows: (1) GbE pretreatment was found to provide a dose-dependent protection against the ethanol-induced gastric ulcers in rats; (2) the GbE pretreatment afforded a dose-dependent inhibition of ethanol-induced depletion of stomach wall mucus, NP-SH contents and increase in the lipid peroxidation (increase MDA) in gastric tissue; (3) gastric ulcer induced by ethanol produced an increase in JNK activity in gastric mucosa which also significantly inhibited by pretreatment with GbE; and (4) GbE alone had no inhibitory effect on gastric secretion in pylorus-ligated rats. CONCLUSION: The finding of this study showed that GbE significantly inhibited the ethanol-induced gastric lesions in rats. We suggest that the preventive effect of GbE may be mediated through: (1) inhibition of lipid peroxidation; (2) preservation of gastric mucus and NP-SH; and (3) blockade of cell apoptosis.

Alcohol levels in Chinese lactating mothers after consumption of alcoholic diet during postpartum "doing-the-month" ritual.

This study examined the effects of exposure to ethanol through cultural practices by lactating mothers. Specifically, the pharmacokinetics of alcohol in Chinese lactating mothers was investigated after they consumed chicken soup flavored with sesame oil and rice wine (CSSR), a typically prescribed diet during the postpartum "doing-the-month" period. Experimental findings were employed to estimate the potential ethanol dose to neonates and determine associated health risks. Twenty-three lactating mothers were examined. Informed consent was obtained from each subject. The target alcohol dosage was 0.3g/kg. Milk and blood samples were collected at fixed time intervals from each subject following exposure to CSSR, and alcohol levels were determined. Acute health risks to infants were estimated by comparing the potential infant dosage to an established criterion dose. Blood alcohol level peaked at 20 min after exposure to CSSR and decreased almost linearly thereafter. Alcohol in milk reached a plateau roughly at 20-40 min after exposure to CSSR and then decreased. Alcohol pharmacokinetics among subjects varied widely. The coefficients of variation in subject alcohol concentrations were 16.5-46.2% (mean, 30.0%) for blood and 32.8-57.6% (mean, 44.4%) for milk. Mean maximal alcohol concentration in blood (30.2+/-5.0 mg/dl) was achieved at 23.5+/-7.6 min and in milk (31.6+/-10.3 mg/dl) at 31.7+/-12.7 min. Potential infant doses were 3.0-58.8 mg (mean, 13.4 mg), and the predicted time required for milk alcohol level to return to zero level was 175 min. The acute health risks for infants exposed to alcohol through their mothers' milk under the current exposure scenario are low (hazard index<0.2). Nursing infants at least 3h after ingesting a diet containing alcohol would further reduce potential health risks.

Effects of Ginkgo biloba extract on cytoprotective factors in rats with duodenal ulcer.

AIM: To investigate the effects of Ginkgo biloba extract on cytoprotective factors in rats with duodenal ulcer. METHODS: Sprague-Dawley rats were randomly divided into four groups: sham operation without ginkgo, sham operation with ginkgo, duodenal ulcer without ginkgo, and duodenal ulcer with ginkgo. Rats with duodenal ulcer were induced by 500 mL/L acetic acid. Rats with ginkgo were intravenously injected with Ginkgo biloba extract from the tail at a dose of 0.5 mg/(kg/d) for 7 and 14 days. RESULTS: Pathological result showed that duodenal ulcer rats with ginkgo improved mucosal healing and inflammation compared with those without ginkgo after 7 d treatment. After 14 d treatment, duodenal ulcer rats with ginkgo significantly increased weight gain (34.0+/-4.5 g versus 24.5+/-9.5 g, P<0.05) compared with those without ginkgo. Duodenal ulcer rats significantly increased cell proliferation (27.4+/-4.0 and 27.8+/-2.3 BrdU-labeled cells in duodenal ulcer rats with and without ginkgo versus 22.4+/-3.5 and 20.8+/-0.5 BrdU-labeled cells in sham operation rats with and without ginkgo, P<0.05) compared with sham operation rats. Mucosal prostaglandin E(2) concentration significantly increased by 129% (P<0.05) in duodenal ulcer rats with ginkgo compared with that in those without ginkgo. Duodenal ulcer rats without ginkgo significantly decreased superoxide dismutase activity in the duodenal mucosa and erythrocytes (19.4+/-6.7 U/mg protein versus 38.1+/-18.9 U/mg protein in the duodenal mucosa, and 4.87+/-1.49 U/mg protein versus 7.78+/-2.16 U/mg protein in erythrocytes, P<0.05) compared with sham operation rats without ginkgo. However, duodenal ulcer rats with ginkgo significantly increased erythrocyte superoxide dismutase activity (8.22+/-1.92 U/mg protein versus 4.87+/-1.49 U/mg protein, P<0.05) compared with those without ginkgo. Duodenal ulcer rats without ginkgo significantly increased plasma lipid peroxides (4.18+/-1.12 micromol/mL versus 1.60+/-1.10 micromol/mL and 1.80+/-0.73 micromol/mL, P<0.05) compared with sham operation rats without ginkgo and duodenal ulcer rats with ginkgo during the experimental period. CONCLUSION: Ginkgo biloba extract can improve weight gain and mucosal healing in duodenal ulcer rats by the actions of cytoprotection and antioxidation.