Effects of fermentable dietary fiber supplementation on oxidative and inflammatory status in hemodialysis patients.

BACKGROUND: Increased oxidative stress, inflammation, and malnutrition are important risk factors for cardiovascular disease in hemodialysis patients. High dietary intake in soluble fiber can decrease the elevated level of serum c-reactive protein in patients with chronic kidney disease. The aim of this study was to evaluate the effect of supplementation of dietary water-soluble fiber on oxidative and inflammatory status in hemodialysis patients. METHODS: In a randomized placebo-controlled trial, we examined the effects of supplementation of dietary fiber on oxidative and inflammatory status in hemodialysis patients. 124 hemodialysis patients were randomly selected and given either 10 g/d, 20 g/d of fiber or placebo for 6 weeks. Anthropometric indices and 24 h diet recall intake was assessed. The CRP, albumin, triglyceride, total cholesterol, LDL, HDL were measured before and after of the intervention. The malondialdehyde (MDA), total antioxidant capacity (T-AOC), Cu-Zn superoxidase dismutase (SOD), glutathione peroxidase (GSH-Px) high-sensitivity C-Reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and interleukin-8 (IL-8) were measured. RESULTS: After 6 weeks of intervention, in 10 g and 20 g/d of fiber supplement groups, TC and LDL level and TC:LDL ratio were significantly decreased, T-AOC was significantly increased, MDA level was significantly deceased, TNF-α, IL-6, IL-8 and CRP level were significantly deceased. TG, HDL, SOD and GSH-Px had no change before and after the intervention. CONCLUSIONS: Dietary fermentable fiber supplementation improved lipid profile and oxidative status, decreased systemic inflammatory state of hemodialysis patients. Thus, it may decrease the risk of cardiovascular events in these patients.

Effects of dietary supplementation with vitamin E and selenium on rat hepatic stellate cell apoptosis.

AIM: To evaluate the effects of dietary supplementation with vitamin E and selenium on proliferation and apoptosis of hepatic stellate cells (HSCs), in acute liver injury induced by CCl(4), and to explore their role in the recovery from hepatic fibrosis phase. METHODS: An acute liver damage model of rats was established by intraperitoneal injection of carbon tetrachloride (0.3 mL/100 g body weight) twice a week, then the rats were killed at 6, 24, 48, and 72 h after the first and third injection, respectively. A liver fibrosis model was established by the same injection for 8 wk. Then three rats were killed at 3, 7, 14, and 28 d after the last injection, respectively. The rats from the intervention group were fed with chow supplemented with vitamin E (250 mg/kg) and selenium (0.2 mg/kg), and the rats in the normal control group and pathological group were given standard chow. Livers were harvested and stained with hematoxylin and eosin, Sirius red. Activated HSCs were determined by alpha-smooth muscle actin immunohistochemistry staining. Apoptotic HSCs were determined by dual staining with the terminal deoxynucleotidyl transferase UTP nick end labeling (TUNEL) and alpha-smooth muscle actin immunohistochemistry. Serum alanine aminotransferase and aspartate aminotransferase were also analyzed. RESULTS: In the acute liver damage model, the degree of liver injury was more serious in the pathological group than in the intervention group. At each time point, the number of activated HSCs was less in the intervention group than in the pathological group, while the number of apoptotic HSCs was more in the intervention group than in the pathological group. In the liver fibrosis model, the degree of liver fibrosis was more serious in the pathological group than in the intervention group. At each time point, the number of activated HSCs was less in the intervention group than in the pathological group, and the number of apoptotic HSCs was more in the intervention group than in the pathological group. CONCLUSION: Vitamin E and selenium supplementation at the given level can inhibit CCl(4)-induced activation and proliferation of HSCs and promote the apoptosis of activated HSCs in acute damage phase. Vitamin E and selenium can also effectively decrease the degree of hepatic fibrosis and promote the recovery process.

[Effect of antioxidant on hepatic stellate cell proliferation and apoptosis during recovery from liver fibrosis].

OBJECTIVE: Effects of dietary supplementation of vitamin E and selenium on proliferation and apoptosis of activated hepatic stellate cell(HSC) were investigated in the rat model of liver fibrosis induced by intraperitoneal injection with CCl4. METHODS: Activated HSC was determined by alpha-smooth muscle actin immunohistochemistry staining and apoptotic HSC determined by dual staining both of the terminal deoxynucleotidyl transferase UTP nick end labeling(TUNEL) and of alpha-smooth muscle actin immunohistochemistry. RESULT: During fibrosis recovery, the number of activated HSCs both in pathological group and in intervention group went down gradually,meanwhile, both the number of apoptotic HSCs and the collagen liver also descend little by little. These data confirmed that HSCs had the core effect on liver fibrogenesis and apoptosis may be a major factor regulating HSCs numbers during the injury-fibrosis-recovery sequence. At each time point, the number of activated HSCs in pathological group is more than intervention group, while apoptotic HSCs are less, which suggested dietary supplement with antioxidative nutrients had effect on HSC apoptosis but more studies are necessary to make the mechanism clearer. CONCLUSION: Dietary supplement with proper vitamin E and selenium can effectively lighten the hepatic fibrosis and promote the recovery of hepatocyte and the degradation of the existing collagens, ie, it is beneficial to the recovery of hepatic fibrosis.