Oxidative stress is considered as a major player in uremia-associated morbidity and mortality in hemodialysis (HD) patients. The aim of this study was to evaluate the effects of turmeric on oxidative stress markers in HD patients. This study was a prospective and double-blind randomized clinical trial. Fifty HD patients aged 18-60 years were recruited after fulfilling the inclusion criteria. Patients were randomly categorized into 2 groups: trial group received turmeric and control group received placebo for 8 weeks. Each patient in the trial group received turmeric, whereas the control group received starch for the same 8 weeks. Plasma malondialdehyde (MDA), red blood cell (RBC) antioxidant enzyme activities as glutathione peroxidase (GPX), glutathione reductase (GR), and catalase (CAT), cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, triglyceride, albumin, and hemoglobin were also measured before and after study. Although MDA level was reduced in both groups, the ratio of decrease was significantly higher in the turmeric group (0.2 vs. 0.1, P = 0.040). Three enzymes of GPX, GR, and CAT levels were increased in both groups; the ratio of increased was significantly higher in the turmeric group for the CAT enzyme (0.73 vs. 0.54; P = 0.02). Also, significant elevation of albumin level in the turmeric group compared with the control group was observed (P = 0.001). Regular ingestion of turmeric reduces plasma MDA and increases RBC CAT activity and plasma albumin levels in HD patients. Turmeric showed no adverse effects.

Background The incidence of accelerated atherosclerosis among patients on hemodialysis is very high and oxidative stress is a potentially major contributor to their morbidity and mortality. Objective To evaluate the effects of Silymarin and/or vitamin E on oxidative stress markers and hemoglobin level in patients on hemodialysis. Methods Eighty patients on hemodialysis were randomized into 4 groups: Group 1 received Silymarin 140 mg 3 times daily; Group 2 received Vitamin E 400 IU/day; Group 3 received Silymarin 140 mg 3 times daily and Vitamin E 400 IU/day; Group 4 was the control. Samples were obtained at baseline and on day 21 for measurement of malondialdehyde (MDA), RBC glutathione peroxidase (GPX), and hemoglobin. Results Combination of Silymarin and vitamin E led to a reduction in the MDA levels (7.84±1.84 vs. 9.20±2.74 nmol/ml; p=0.008). There was a significant increase in RBC GPX levels in all treatment groups compared to controls after 3 weeks. This was more pronounced in the group receiving combination compared to vitamin E or the control group (5.78±3.51, 4.22±1.63, and 3.16±1.89 Iu/gr-Hb respectively; p<0.001). There was also a significant increase in mean hemoglobin of all treatment groups compared to control. Conclusions Oral supplementation with Silymarin and vitamin E leads to reduction in MDA, increase in RBC GPX and increase in hemoglobin levels in patients with ESRD. Studies with larger sample sizes and longer follow-up are required to investigate the effect of Silymarin on cardiovascular outcomes, and erythropoietin requirement.

Objectives:To investigate the effect of silymarin and milk thistle extract on the progression of diabetic nephropathy (DN) in rats. Methods: Diabetes was induced with a single intraperitoneal (IP) injection of streptozotocin (STZ) (60 mg/kg). Silymarin (100 mg/kg/d) or the extract (1.2 g/kg/d) was gavaged for 4 weeks. Blood glucose (BS), serum urea (S u ), serum creatinine (S cr ), and 24-h urine protein (Up) were measured and glomerular filtration rate (GFR) was calculated. Concentration of thiobarbituric acid reactive species (TBARS) and activities of glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) were evaluated in the renal tissue. Results: Data were expressed as mean ± SEM. Silymarin or the extract had no significant effect on BS, S cr , and GFR. Both milk thistle extract and silymarin, respectively, decreased S u (mg/dL) (87.1 ± 7.78, p < 0.001; 84.5 ± 7.15, p < 0.001), Up (mg) (5.22 ± 1.56, p = 0.014; 5.67 ± 0.86, p = 0.034), and tissue TBARS (nmol/mg protein) (0.67 ± 0.04, p < 0.001; 0.63 ± 0.07, p < 0.001) in diabetic rats, compared to diabetic control (DC) (S u : 131.0 ± 4.55, Up: 8.3 ± 0.84, TBARS: 0.94 ± 0.06). Both the extract and silymarin could increase the activity of CAT (IU/mg protein) (25.5 ± 4.0, p = 0.005; 20 ± 1.8, p = 0.16) and GPx (IU/mg protein) (0.86 ± 0.05, p = 0.005; 0.74 ± 0.04, p = 0.10), respectively, in diabetic rats compared to DC (CAT = 14.4 ± 2.0, GPx = 0.57 ± 0.02). Conclusion: Milk thistle extract, to a lesser extent silymarin, can attenuate DN in rats possibly by increasing kidney CAT and GPx activity and decreasing lipid peroxidation in renal tissue.

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Background: Berberine is a well-known alkaloid derived from Berberis species. Objectives: The present study aimed to investigate the hepatoprotective properties of berberine and elucidate its probable mechanisms against sodium nitrite toxicity. Methods: Forty animals were randomly classified into five equal groups to be treated for 60 days, including group 1: Control, group 2: Berberine-treated (100 mg/kg), group 3: Sodium nitrite-treated (80 mg/kg), group 4: Sodium nitrite together with 50 mg/kg of berberine, and group 5: Sodium nitrite together with 100 mg/kg of berberine. The protective effects of berberine against sodium nitrite induced-liver damage were investigated using parameters related to oxidative stress, inflammation, fibrosis, and apoptosis in the hepatocytes. Results: Treatment of rats with sodium nitrite considerably increased alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities, malondialdehyde (MDA) content, tumor necrosis factor (TNF)-α expression, caspase-3 activity, and transforming growth factor (TGF)-β1 concentration (P < 0.05) and significantly declined the levels of reduced glutathione (GSH), glutathione reductase (GR), glutathione S-transferase (GST), and glutathione peroxidase (GPx) (P < 0.05). The treatment of intoxicated rats with 100 mg/kg of berberine significantly reversed these changes and reached the values approximately to the normal level. However, berberine 50 mg/kg failed to normalize the disturbances. Conclusions: This study demonstrated that berberine could decrease sodium nitrite-induced liver injury in a dose-dependent manner probably due to its antioxidant, anti-inflammatory, anti-apoptotic, and antifibrotic capacities.