Previous studies have shown that inflammatory factors increases in pregnancy and is associated with several complications of pregnancy. The aim of this study was to assess effects of daily consumption of probiotic yoghurt on inflammatory factors in pregnant women. In a randomized clinical trial, seventy primigravid (the first pregnancy) and singleton pregnant women aged 18-30 years were assigned to two groups. Subjects consumed daily 200 g probiotic yoghurt containing Lactobacillus acidophilus La5 and Bifidobacterium animalis BB12 (10(7) CFU g(-1) for each) or 200 g conventional yoghurt for 9 weeks. Fasting blood samples were collected at baseline (28 weeks of gestation) and after intervention (37 weeks of gestation). Inflammatory factors, hs-CRP and TNF-alpha, were measured by Enzyme-linked Immunosorbent Assay (ELISA). Independent t-test was used to compare the two groups after intervention and paired-sample t-test compared variables before and after treatment. The results showed that the probiotic yogurt brought about a decrease in the serum hs-CRP level, from 10.44 +/- 1.56 to 7.44 +/- 1.03 microg mL(-1) (p = 0.041). There was no significant change in the conventional yogurt group in the serum hs-CRP level (12.55 +/- 1.57 to 14.51 +/- 1.62 microg mL(-1), p = 0.202). The probiotic yogurt had no effect on TNF-alpha (from 73.75 +/- 6.59 to 77.91 +/- 5.61 pg mL(-1), p = 0.633). Serum TNF-alpha did not change in the conventional yogurt group (p = 0.134). In conclusion probiotic yogurt significantly decreased hs-CRP in pregnant women but had no effect on TNF-alpha.

Introduction. Diabetic nephropathy is one of the leading causes of end‐stage renal disease worldwide. Uncontrolled hyperglycemia and subsequent production of glycation end‐products activate the paths which lead to diabetic nephropathy. The aim of this study was to assess the effects of L‐lysine on antioxidant capacity, biochemical factors, kidney function, HSP70 level, and the expression of the TGFβ, VEGF, and RAGE genes in rats with streptozocin‐induced diabetes mellitus. Methods. Thirty‐two male Wistar rats were randomly allocated to four eight‐rat groups, namely, a healthy group, a diabetic group treated with vehicle (DM + vehicle), a diabetic group treated with L‐lysine (DM + Lys), and a healthy group treated with L‐lysine (healthy + Lys). Rats in the DM + Lys and the healthy + Lys groups were treated with L‐lysine 0.15%. The levels of fasting blood glucose, insulin, HbA_1C, advanced glycation end‐products (AGEs), lipid profile, serum creatinine, blood urea nitrogen, glomerular filtration rate, urine microalbumin, oxidative stress parameters, kidney histology and morphology, and TGFβ, VEGF, and RAGE gene expressions were assessed. Findings. An eight‐week treatment with L‐lysine significantly reduced the levels of fasting blood glucose, AGEs, kidney function parameters, oxidative stress parameters, lipid profile, and the TGFβ, VEGF, and RAGE gene expression and significantly increased the levels of serum insulin and tissue HSP70. Conclusion. Treatment with L‐lysine seems to slow down the progression of diabetic nephropathy.

Introduction. Bile duct ligation (BDL) and subsequent cholestasis are associated with oxidative stress and liver injury and fibrosis. Hesperidin (3,5,7‐trihydroxyflavanone 7‐rhamnoglucoside) is a flavanone glycoside abundant in citrus fruits. It has positive effects on diabetic retinopathy, reduced platelet aggregation, and blood flow alterations and has the potential to reduce liver injury in oxidative stress. The aim of this study was to evaluate the hepatoprotective effects of hesperidin on BDL‐induced liver injury in rats. Methods. A total of 48 adult male Wistar rats were equally allocated to six eight‐rat groups, namely, a healthy group, a sham group, a BDL+Vehicle group (BDL plus treatment with distilled water), a BDL+VitC group (BDL plus treatment with vitamin C 4.25 μg/kg), a BDL+Hesp100 group (BDL plus treatment with hesperidin 100 mg/kg/day), and a BDL+Hesp200 group (BDL plus treatment with hesperidin 200 mg/kg/day). Treatments were orally provided for 21 consecutive days. Finally, rats were sacrificed through heart blood sampling. Blood samples were centrifuged, and liver function, oxidative stress, and antioxidant parameters were assessed. Liver tissue was also assessed for oxidative stress, antioxidant, and histological parameters. The expression of inflammatory genes, namely, TGFβ1, iNOS, Caspase‐3, and α‐SMA, was measured through polymerase chain reaction. Findings. Hesperidin supplementation was associated with significant decrease in the levels of liver enzymes, bilirubin, nitric oxide, malondialdehyde, protein carbonyl, and inflammatory gene expression; significant increase in the levels of total antioxidant capacity, glutathione, and superoxide dismutase and catalase enzyme activity; and significant improvement in the histological morphology and structure of the liver parenchyma. Conclusion. Hesperidin has significant positive effects on liver morphology and structure, inflammation, fibrosis, and oxidative stress in rats with BDL‐induced cholestatic liver injury.

Islet amyloid formation causes destruction of insulin-producing beta-cells of the pancreas. The subsequent lack of insulin leads to increased blood and urine glucose. In this research, the fluorimetric assay was used to examine the effects of aluminium and some nutritionally essential trace elements including, manganese, copper and selenium on amyloid formation of human peptide of amylin under near-physiological circumstances. Results obtained from in vitro study showed that after 120 h incubation by shaker incubator in 37 degrees C, copper and selenium at 8 microM inhibited amylin 8 microM from amyloid fibril formation by 22.1 and 11.3%, respectively (p<0.05) while the similar values of either aluminium and manganese promoted the formation of beta-pleated sheet structure by 19.3 and 13.2% respectively (p<0.05). If islet amyloid is cytotoxic to beta-cells then copper and selenium may be able to protect these cells against degeneration in diabetic patients especially in type 2 diabetes mellitus.