Nielsengoode8042

Acrylamide is a toxic compound that forms during food processing at high temperatures. Acrylamide has been shown to induce toxicity in various organs in the body. This study aimed to investigate the effect of acrylamide exposure on the susceptibility of the colon to ulcerative colitis in a mouse model.

Mice were pretreated with acrylamide (oral, 20 and 30 mg/kg/day) for 21 consecutive days, and colitis was induced by intrarectal administration of acetic acid.

The results revealed that acrylamide-pretreatment significantly increased disease activity index (DAI), macroscopic damage, histological changes of the colonic mucosa and oxidative stress markers carbonyl protein, malondialdehyde (MDA), and nitric oxide (NO), whereas it decreased the levels of anti-oxidants glutathione (GSH), superoxide dismutase (SOD) and catalase. Moreover, induction of colitis in acrylamide-pretreated mice caused a higher increase in colonic levels of myeloperoxidase (MPO), matrix metalloproteinase (MMP)-9, monocyte chemoattractant protein (MCP)-1, cytochrome-c, caspase-3, proinflammatory cytokine tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and interferon (IFN)-γ, whereas it reduced the level of IL-10. The mRNA expression of nuclear factor kappa B (NF-κB) and inducible nitric oxide synthase (iNOS) were further increased in colon tissue of mice exposed to acrylamide.

These findings suggest that acrylamide can accelerate the development of acetic acid-induced colitis. In conclusion, chronic acrylamide exposure may aggravate the severity of ulcerative colitis and increase colonic mucosal damage through oxidative stress and inflammatory responses.

These findings suggest that acrylamide can accelerate the development of acetic acid-induced colitis. In conclusion, chronic acrylamide exposure may aggravate the severity of ulcerative colitis and increase colonic mucosal damage through oxidative stress and inflammatory responses.

Hypercholesterolemia is correlated with brain amyloid-β (Aβ) deposition and impaired cognitive functions and contributes to Alzheimer's disease. Effects of cholesterol-lowering dill tablets and aqueous extract of

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(basil) on learning and memory and hippocampus fatty acid composition were examined. mRNA levels of the genes involved in cholesterol homeostasis were also determined in high-cholesterol diet (HCD) fed rats.

Forty male Wistar rats were allocated to 4 groups rats fed chow diet (C); rats fed high-cholesterol (2%) diet (HCD); rats treated with HCD+300 mg/kg dill tablets (HCD+Dill); and finally, rats fed HCD and treated with 400 mg/kg basil aqueous extract (HCD+basil). Treatment was carried out for 16 weeks. Hippocampus Aβ(1-42) level was determined. Spatial and passive avoidance tests were used to examine cognitive functions. Hippocampal FA composition was assessed by gas chromatography. Basil aqueous extract was analyzed by GC-double mass spectroscopy (GC-MS/MS) and expression of LXR-α, LXR-β, and ABCA1 genes was assessed by qRT-PCR.

Dill tablets and basil extract remarkably ameliorated serum cholesterol (

<0.001), retarded hippocampal accumulation of Aβ, and attenuated HCD-induced memory impairment. Hippocampus FA composition did not change but serum cholesterol was found positively correlated with hippocampus Aβ(1-42) (

<0.001), total n 6 PUFA (

=0.013), and Aβ(1-42) showed correlation with the ratio of n6 to n3 PUFA. At least 70 components were identified in basil aqueous extract.

Dill tablets and aqueous extract of basil attenuated the hypercholesterolemia-induced memory impairment by lowering serum cholesterol and hippocampus amyloid deposits, and probably beneficial in AD adjuvant therapy.

Dill tablets and aqueous extract of basil attenuated the hypercholesterolemia-induced memory impairment by lowering serum cholesterol and hippocampus amyloid deposits, and probably beneficial in AD adjuvant therapy.

Metabolic syndrome (MS) is a cause of death worldwide. The hepatic nuclear factor- NF-kβ (NF-kβ) is the cardinal player of hepatic homeostasis, insulin sensitivity, and lipid metabolism. Thus, we investigated the effect of thiamine on hepatic gene expression of NF-kβ and its levels of activators in MS rats.

Male Wistar rats were randomly divided into 4 equal groups (ten rats in each group) normal, MS, and two alike groups under thiamine treatment. MS was induced in rats with a high sucrose solution (40 % in drinking water) for 4 months. Treated groups of rats received 0.18 % of thiamine daily in drinking water. Hematoxylin-Eosin stains were employed to determine the histopathological changes of the liver. Metabolic profile, glycation products, oxidative stress, inflammatory markers, the activity of glyoxalase-I, as well as NF-kβ hepatic expression of all rat groups, were determined.

Acute hepatitis was not observed in the livers of the thiamine treated MS rats. Besides, the treatment showed an advantageous effect on glucose, lipid metabolism, and body weight via down-regulation of hepatic NF-kβ and induction of glyoxalase system activity. Furthermore, the treatment decreased diverse glycation, oxidative stress, and inflammatory markers (

>0.001).

Thiamine decreased body weight and improved metabolism and activity of glyoxalase-I in MS rats with anti-glycation, antioxidant, and anti-inflammatory activities. Further, the treatment had a hepato-protective effect via reduction of NF-kβ signaling.

Thiamine decreased body weight and improved metabolism and activity of glyoxalase-I in MS rats with anti-glycation, antioxidant, and anti-inflammatory activities. Further, the treatment had a hepato-protective effect via reduction of NF-kβ signaling.Metabolic syndrome is a condition associated with obesity, diabetes, dyslipidemia, and high blood pressure. Recently, the use of phytochemicals is suggested in the control and treatment of metabolic syndrome. The Azadirachta indica (neem) is an evergreen tree belonging to the family of Meliaceae. Multiple studies have been confirmed the anti-diabetic and anti-hypertension, anti-hyperlipidemia, and anti-obesity effects of neem. In this review, we reported the protective effects of neem against the complications of metabolic syndrome with a special focus on mechanisms that are involved. It has been shown that neem can control hyperglycemia and hypertension through over-expression of transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) and anti-oxidant effects. Neem also reduced the glucose uptake through up-regulation of glucose transporter 4 (GLUT4) and inhibition of key intestinal enzymes such as glucosidases. Selleck LY2090314 Moreover, neem showed anti-hypertensive effects possibility via the block of calcium channels, up-regulation of endothelial nitric oxide synthase (eNOS), and extracellular signal-regulated kinases 1/2 (ERK1/2) signaling pathway.