Expression Levels Of Tumor Necrosis Factor-α Research Articles

Ethanol extracts of Isochrysis zhanjiangensis alleviate acute alcoholic liver injury and modulate intestinal bacteria dysbiosis in mice.

Alcoholic liver disease (ALD) is responsible for 3.3 million deaths per annum. Efficacious therapeutic modalities or drug treatments for ALD have not yet been found, so it is urgent to seek new agents for preventing ALD and its related disease. Many experiments have indicated that modulating the gut microbiota and regulating the toll-like receptor 4 (TLR4)/nuclear transcription factor-κB (NF-κB) inflammatory pathway can provide a new target for prevention and treatment of ALD. Marine microalgae have their natural metabolic pathways to synthesize various of bioactive compounds as promising candidates for hepatoprotection. In this study, we investigated ethanol extracts from Isochrysis zhanjiangensis (EEIZ) to evaluate their ability to alleviate acute alcoholic liver injury, regulate TLR4/NF-κB inflammatory pathway and modulate intestinal bacteria dysbiosis in mice for ALD treatment. In the acute ALD mouse model, EEIZ reduced levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, triacylglyceride, total cholesterol and low-density lipoprotein, while increasing the level of high-density lipoprotein. Besides, TLR4, myeloid differentiation factor 88, NF-κB and tumor necrosis factor-α expression levels in liver tissue were effectively downregulated by EEIZ. Furthermore, treatment with EEIZ enhanced intestinal homeostasis and significantly alleviated the damage caused by alcohol. EEIZ showed effective hepatoprotective activity against alcohol-induced acute liver injury in mice as it could alleviate hepatocyte damage, suppress the TLR4/NF-κB inflammatory pathway and regulate the intestinal flora structure. EEIZ could be a good candidate for preventing acute alcoholic liver injury. © 2024 Society of Chemical Industry.

Resveratrol ameliorates oxidative stress, inflammatory response and lipid metabolism in common carp (Cyprinus carpio) fed with high-fat diet

High-fat diet is regarded as crucial inducers of oxidative stress, inflammation, and metabolic imbalance. In order to investigate the ameliorative potential of resveratrol against the progression of liver injury towards steatohepatitis, common carp (Cyprinus carpio) were distributed into six experimental groups and were fed with a normal-fat diet, a high-fat diet, and supplemented with resveratrol (0.8, 1.6, 2.4, and 3.2 g/kg diet) for 8 weeks. The high-fat diet decreased the antioxidant capacities, as well as causing the inflammatory response and lipid deposition of common carp. Resveratrol induced a marked elevation in the final body weight, weight gain rate, condition factor and significant decrease in the feed conversion ratio. Moreover, dietary resveratrol showed a significant decrease in the alanine aminotransferase, aspartate aminotransferase, triglyceride and low-density lipoprotein levels, which was accompanied by an increase in high-density lipoprotein concentration in serum. A significant elevation in total superoxide dismutase, catalase, glutathione peroxidase and a decreased malondialdehyde content were observed, along with a substantial elevation in antioxidant activities were found. Additionally, fish fed with resveratrol had an up-regulation of hepatic catalase, copper, zinc superoxide dismutase, glutathione peroxidase 1a, and glutathione peroxidase 1b gene expression via Nrf2 signaling pathway. Expectedly, our results also demonstrated that resveratrol regulates hepatic lipid metabolism in fish by inhibiting the expression of hepatic lipogenesis genes (acetyl-CoA carboxylase 1, fatty acid synthase, and sterol regulatory element binding protein 1), fatty acid uptake-related genes of lipoprotein lipase, and β-oxidation-related genes via PPAR-γ signaling pathway. Furthermore, dietary resveratrol reduced inflammation, as evident by down-regulating the interleukin-1β, interleukin-6, interleukin-8, and tumor necrosis factor-α expression levels and upregulating the interleukin-10 and transforming growth factor-β2 expression levels via NF-κB signaling pathway. As a whole, our results demonstrated that resveratrol defensed the impacts against high-fat diet on the serum biochemical, hepatic antioxidants, inflammation, and lipid metabolism.

The growth performance and non-specific immunity of juvenile grass carp (Ctenopharyngodon idella) affected by dietary alginate oligosaccharide.

The effects of alginate oligosaccharides (AOs) on the growth performance and non-specific immunity of juvenile grass carp (Ctenopharyngodon idella) were investigated by performing a 60-day feeding trial. Four trial diets were formulated and supplemented with different doses of AOs (0, 100, 200 and 400mg/kg). Triplicate groups of grass carp were fed with one of the diets twice daily. The grass carps fed with diets containing an appropriate dose of AOs for 60days exhibited higher survival rates; body weight gains; specific growth rates; resistance to Aeromonas hydrophila; superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase activities; and serum total protein, lysozyme, alkaline phosphatase, complement C3, complement C4 and interleukin-10 expression levels and lower feed conversion ratios and malondialdehyde, alanine aminotransferase, aspartate aminotransferase, IL-1β expression, IL-8 expression and tumor necrosis factor-α expression levels than the control group (p < 0.05). Based on the effects of AOs on growth performance and survival percent, the optimum dose of AOs was 200mg/kg. Results indicate that AOs as a dietary supplement enhances the growth performance and non-specific immunity of grass carps and their resistance to diseases.

Protective Role of Coenzyme Q10 in Acute Sepsis-Induced Liver Injury in BALB/c Mice.

Sepsis increases the risk of the liver injury development. According to the research works, coenzyme Q10 exhibits hepatoprotective properties in vivo as well as in vitro. Current work aimed at investigating the protective impacts of coenzyme Q10 against liver injury in septic BALB/c mice. The male BALB/c mice were randomly segregated into 4 groups: the control group, the coenzyme Q10 treatment group, the puncture and cecal ligation group, and the coenzyme Q10+cecal ligation and puncture group. Cecal ligation and puncture was conducted after gavagaging the mice with coenzyme Q10 during two weeks. Following 48 h postcecal ligation and puncture, we estimated hepatic biochemical parameters and histopathological changes in hepatic tissue. We evaluated the expression of factors associated with autophagy, pyroptosis, and inflammation. Findings indicated that coenzyme Q10 decreased the plasma levels in alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase in the cecal ligation and puncture group. Coenzyme Q10 significantly inhibited the elevation of sequestosome-1, interleukin-1β, oligomerization domain-like receptor 3 and nucleotide-binding, interleukin-6, and tumor necrosis factor-α expression levels; coenzyme Q10 also increased beclin 1 levels. Coenzyme Q10 might be a significant agent in the treatment of liver injury induced by sepsis.

Pterostilbene protects against acute renal ischemia reperfusion injury and inhibits oxidative stress, inducible nitric oxide synthase expression and inflammation in rats via the Toll-like receptor 4/nuclear factor-κB signaling pathway.

Previous studies have demonstrated that pterostilbene (Pter) prevents oxidative stress, suppresses cell growth and exhibits anti-fungal and anti-inflammatory effects. Pter is used to treat a number of clinical diseases, including Alzheimer's disease, various malignancies and hypercholesteremia. The aim of the present study was to investigate whether Pter protects against acute renal ischemia reperfusion injury (IRI) and inhibits oxidative stress, inducible nitric oxide synthase (iNOS) expression and inflammation in rats. A total of 40 adult male Sprague Dawley rats were divided into the following 5 groups at random: Control group, where rats were not subjected to renal IRI; IRI group, where rats were subjected to renal IRI; Pter 10 group, where rats underwent renal IRI and were treated with 10 mg/kg Pter; Pter 20 group, where rats underwent renal IRI and were treated with 20 mg/kg Pter; Pter 30 group, where rats underwent renal IRI and were treated with 30 mg/kg Pter. The results demonstrated that Pter treatment improved renal function following acute renal IRI. Compared with the untreated renal IRI group, myeloperoxidase, iNOS, interleukin (IL)-1β, IL-6 and tumor necrosis factor-α expression levels were significantly decreased (P<0.01), whereas IL-10 expression levels were significantly increased (P<0.01) following treatment with Pter in acute renal IRI rats. In addition, Pter significantly attenuated caspase-3 activity and the Toll-like receptor 4 (TLR4)/nuclear factor (NF)-κB signaling pathway induced by acute renal IRI (P<0.01). These results provide evidence to suggest that administration of Pter may protect against acute renal IRI and inhibit oxidative stress, iNOS expression and inflammation in rats via the TLR4/NF-κB signaling pathway.

HIV-Specific CD8+ T Cell–Mediated Viral Suppression Correlates With the Expression of CD57

Virus-specific CD8(+) T-cell responses are believed to play an important role in the control of HIV-1 infection; however, what constitutes an effective HIV-1 CD8(+) T-cell response remains a topic of debate. The ex vivo viral suppressive capacity was measured of CD8(+) T cells from 44 HIV-1-positive individuals. The phenotypic and cytokine profiles, and also the specificity of the CD8(+) T cells, were correlated with the suppression of HIV-1 replication. We also aimed to determine whether antiretroviral therapy (ART) had any positive effect on the HIV-1 suppressive CD8(+) T cells. Ex vivo suppression assay was used to evaluate the ability of CD8(+) T cells to suppress HIV-1 replication in autologous CD4(+) T cells. The CD107a, interferon-γ, interleukin-2, tumor necrosis factor-α (TNF-α), and macrophage inflammatory protein-1β (MIP-1β) responses to HIV-1 were evaluated by intracellular staining. The phenotypic profile of CD8(+) T cells was determined by whole blood staining. The expression of CD57 on effector CD8(+) T cells correlated with the suppression of HIV-1 replication and to the duration of ART. CD107a and tumor necrosis factor-α expression levels were significantly higher in individuals with ex vivo suppressive activity compared with individuals without suppressive activity. Standard in vitro assays measuring one or several cytokines do not correlate with the functional viral suppressive capacity of CD8(+) T cells from HIV-1-positive individuals. The best correlation of viral suppression was found to be CD57 expression. CD57 expression correlated with the duration of ART, suggesting that ART restores the cytotoxic capacity of CD8(+) T lymphocytes.

Effects of fatigue from sleep deprivation on experimental periodontitis in rats

Factors such as vascularization of the periodontium, inflammatory reactions and immune response affect the oral environment and ecology, decreasing host resistance and promoting the development of symptoms and the advancement of periodontal disease. Fatigue also influences the hypothalamic-pituitary-adrenal axis and reports relate it to systemic resistance. The aim of this study was to evaluate whether fatigue is a modifying factor for periodontal disease in rats. We divided 24 3-wk-old male Sprague-Dawley rats randomly into the following four groups: control; fatigue (deep sleep deprivation for 7 d); infection (rats inoculated with carboxymethyl cellulose containing periodontopathic bacteria); and compound (combined fatigue and infection conditions). Weight, serum corticosterone levels, serum albumin levels, interleukin-1β and tumor necrosis factor-α expression levels and distance from the cement-enamel junction to the alveolar bone crest were measured at baseline, and on the 36th (before sleep deprivation), 43rd (immediately after sleep deprivation) and 57th d (end of experiment). Immediately after sleep deprivation and at the end of the experiment, weight gain in the fatigue and compound groups was significantly lower than in controls (p < 0.05). Immediately after sleep deprivation, serum corticosterone levels were significantly higher in the fatigue and compound groups than in controls (p < 0.05). Moreover, serum albumin levels were significantly lower in the fatigue and compound groups than in controls (p < 0.05). Immediately after sleep deprivation, gene expression of interleukin-1β was significantly higher in the infection and compound groups than in controls (p < 0.05). Moreover, gene expression of tumor necrosis factor-α was significantly higher in the compound group than in controls (p < 0.05). At the end of the experiment, the distance from the cement-enamel junction to the alveolar bone crest was significantly higher in the infection and compound groups than in controls (p < 0.05). Moreover, the distance was significantly higher in the compound group than in the infection group. Fatigue worsened systemic health in rats and increased gingival inflammation and alveolar bone loss in experimental periodontitis. In conclusion, our results suggest that fatigue is a modifying factor for periodontal disease in rats.

Neuroprotective effect of forsythiaside against transient cerebral global ischemia in gerbil

Forsythiaside, a phenylethanoside, has been reported to have anti-oxidative activity and memory ameliorating effects against a scopolamine-induced memory deficit model. The aim of this study was to determine whether forsythiaside has neuroprotective activity on transient cerebral global ischemia in gerbil. Transient cerebral ischemia was induced by bilateral common carotid artery occlusion for 5min and followed by reperfusion for 7days. Oral administration of forsythiaside was conducted immediately after reperfusion and once a day over the next 7days. The forsythiaside administration significantly increased the number of viable neurons detected by neuronal nuclei immunostaining and decreased degenerating neuronal cells detected by Fluoro-Jade B staining in the hippocampal CA1 region, at the 7th day post-ischemia (P<0.05). Forsythiaside also significantly decreased the number of ionized calcium-binding adaptor molecule-1-detected activated microglia and glial fibrillary acidic protein-detected astrocytes, both of which were increased after ischemic insults, and decreased interleukin-1β and tumor necrosis factor-α expression levels, which were also increased after the insults (P<0.05). In addition, forsythiaside significantly improved ischemia-induced cognitive impairments in the Y-maze task (P<0.05). These results suggest that forsythiaside exhibits neuroprotective properties, which are, in part, mediated by its anti-inflammatory activities supported by forsythiaside-induced reductions of activated glial cells and expression levels of interleukin-1β and tumor necrosis factor-α.