Nanotechnology applications for treatment of hepatic infections via modulating Hepatic histopathological and DNA alterations.

BACKGROUND: Nanoparticles are recently playing a potential role in improving drug uptake and the treatment of diseases. A variety of nanoparticles, such as selenium nanoparticles (SeNPs) and Silver nanoparticles (AgNPs) have been used as drug carriers in various ways for treatment of cancers and liver diseases. Our aim in this study is to investigate the ability of AgNPs and SeNPs to target and treat the viral and bacterial infection of liver in rats and cell lines. METHODS: For assessment of antioxidant activity of silver nanoparticles, six adult male albino rats were included in this study, liver slices were taken and assigned to 6 groups. Markers of hepatic functions, oxidative stress and inflammation in liver slices are carried out. While for assessment of antiviral activity of SeNPs, HBV-replicating human cell line HepG2 and normal human cell lines were used, hepatic and inflammatory alterations are determined through quantitative polymerase chain reaction (PCR) and comet assay techniques. RESULTS: The effect of Ag-NPs on interleukin-6 (IL-6) and tumor necrosis factor (TNF-α) levels were reduced in different treated groups with Ag-NPs compared with the control and diseased groups. On the other hand, SeNPs revealed significant alterations in the inflammatory markers as well as DNA damage in the treated HBV- human cell line HepG2 compared to the diseased ones. CONCLUSION: Silver nanoparticles have the ability for producing various hepatic alterations and can inhibit the proliferation of hepatic stellate cells (HSCs) in a dose and size dependent manner. On the other hand, SeNPs showed excellent selectivity towards viral cells in the HepG2 cell lines. Both Ag-NPs and SeNPs might be a promising drug design for treating viral and bacterial liver diseases.

Selenium and silver nanoparticles: A new approach for treatment of bacterial and viral hepatic infections via modulating oxidative stress and DNA fragmentation.

Nanoparticles are recently playing a potential role in improving drug uptake and the treatment of diseases. A variety of nanoparticles, such as selenium nanoparticles (SeNPs) and silver nanoparticles (AgNPs) have been used as drug carriers in various ways for treatment of cancers and liver diseases. Our aim in this study is to investigate the ability of AgNPs and SeNPs to target and treat the viral and bacterial infection of the liver in rats and cell lines. For assessment of antioxidant activity of AgNPs in rats with induced liver bacterial infection, six adult male albino rats were included in this study, liver slices were taken and assigned to 6 groups. Markers of hepatic functions, oxidative stress, and inflammation in liver slices are carried out. Although for assessment of antiviral activity of SeNPs, hepatitis B virus transfected (HBV)-replicating human cell line HepG2 and normal hepatocyte cells were used, hepatic and inflammatory alterations are determined through quantitative polymerase chain reaction and comet assay techniques. The effect of AgNPs on interleukin-6 and tumor necrosis factor levels were reduced in different treated groups with AgNPs compared with the control and diseased groups. On the other hand, SeNPs revealed significant alterations in the inflammatory markers as well as DNA damage in the treated HBV-human cell line HepG2 compared to the diseased ones. AgNPs have the ability for producing various hepatic alterations and can inhibit the proliferation of hepatic stellate cells (HSCs) in a dose and size-dependent manner. On the other hand, SeNPs showed excellent selectivity towards viral cells in the HepG2 cell lines. Both AgNPs and SeNPs might be promising drug designs for treating viral and bacterial liver diseases.

The Relevance of Single-nucleotide Polymorphism +62 G>A to the Expression of Resistin Gene Affecting Serum Resistin Levels in Metabolic Syndrome in the Egyptian Population.

BACKGROUND: Metabolic Syndrome (MS) is a clinical condition consisting of risk factors associated with type two diabetes and developing cardiovascular disease. It has been suggested that resistin is a linkage between obesity, inflammation and type two diabetes. This study aims to investigate whether Resistin Gene (RETN) polymorphism (+62G>A) is linked to MS and resistin levels among the Egyptian population. METHODS: This study was performed with 310 Egyptian volunteers: 160 MS subjects and 150 controls. Anthropometric parameters and biochemical variables were determined. The RETN +62G>A polymorphism was genotyped by PCR-RFLP technique. RESULTS: The resistin levels of the MS group were significantly higher than those of the control group. Resistin levels were positively correlated with anthropometric parameters and liver biomarkers in the MS group. According to RETN +62G>A polymorphism, carriers with the A allele (GA/AA) had significantly increased resistin levels than subjects with the GG genotype, consequently, the RETN +62G >A polymorphism was found to be related to MS, biochemical parameters and anthropometric variables. CONCLUSION: These findings propose that the RETN +62G>A polymorphism has a great impact on the circulating resistin concentrations, and that resistin levels are strongly related to MS. Therefore, this RETN polymorphism is related to the risk of the prevalence of MS in the Egyptians.

The Protective Effect of Korean Red Ginseng Against Rotenone-Induced Parkinson's Disease in Rat Model: Modulation of Nuclear Factor-κß and Caspase-3.

OBJECTIVE: Korean red ginseng was reported to have many biological effects like the antioxidant and the anti-inflammatory activities. Oxidative stress and neuro-inflammation play major roles in the pathogenesis of Parkinson's disease (PD). The current study aimed to investigate the protective effects of ginseng on rotenone-induced PD in rats. METHODS: Rats were randomly allocated into 4 groups: normal rats, rotenone control, ginseng+rotenone and ginseng only treated rats. The severity of PD was evaluated through locomotor activity perceived in the open field test, histological examination and immunohistochemical detection of amyloid-ß in brain tissues, in addition to the biochemical assessment of tyrosine hydroxylase activity in brain tissues. Moreover, the following parameters were investigated for studying the possible mechanisms of ginseng neuroprotective effect: nuclear factor-κß (NF-κß), tumor necrosis factor-alpha (TNF-α), caspase- 3, lipid peroxides and reduced glutathione (GSH). RESULTS: Ginseng exhibited potent neuroprotective effect that was reflected upon the histopathological examination, marked improvement in the locomotor activity and through its ability to suppress the amyloid- ß deposition in the cortex and striatum along with significant increase in the tyrosine hydroxylase activity. Ginseng successfully inhibited the NF-κß inflammatory pathway in brain tissues beside the inhibition of other oxidative stress and inflammatory mediators. Furthermore, it exhibited antiapoptotic effect via the inhibition of caspase-3 expression. CONCLUSION: Ginseng could be a promising treatment in PD. It can suppress dopaminergic neuron degeneration through variable mechanisms mainly via inhibition of NF-κß pathway in addition to inhibition of oxidative stress and apoptosis.

Adiponectin and sE-selectin concentrations in relation to inflammation in obese type 2 diabetic patients with coronary heart disease.

Adipose tissue can release proinflammatory mediators, namely C-reactive protein (CRP), interleukin 1ß (IL-1ß), and monocyte chemotactic protein 1 (MCP-1), contributing to vascular injury and insulin resistance (IR). Other mediators namely, adiponectin and nitric oxide (NO) are protective. We enrolled type 2 diabetes mellitus (T2DM) obese male patients without coronary heart disease ([CHD] group II, n = 25) and T2DM obese patients with CHD (group III, n = 25). They were compared with 20 age- and body mass index (BMI)-matched nondiabetic control males (group I). Fasting blood glucose (FBG), glycated hemoglobin (HbA(1c)%), lipids, insulin, malondialdehyde ([MDA]; lipid peroxidation product), NO, high-sensitivity CRP (hsCRP), IL-1ß, MCP-1, adiponectin as well as sE-selectin concentration were significantly different in patients with T2DM and CHD compared with patients without CHD and nondiabetic controls (P = .01). There was a significant negative correlation between adiponectin and E-selectin (P = .0001). Adipose tissue in T2DM obese patients may contribute to the pathogenesis of CHD.

Adiponectin and pro-inflammatory cytokines in obese diabetic boys.

Adiponectin serum levels were significantly lower in obese diabetic than in non-obese healthy boys (P <0.001). Circulating soluble E-selectin levels was significantly higher in obese diabetic boys than the healthy non-obese (P <0.01). There were significant inverse correlations between adiponectin and sE-selectin, hsCRP, IL-1b, and MCP-1 and positively with NOx. We conclude that sE-selectin and MCP-1 may represent a link between obesity and related co-morbidities in children and adults.