scholarly journals Antioxidant Capacity-Related Preventive Effects of Shoumei (Slightly Fermented Camellia sinensis) Polyphenols against Hepatic Injury

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Ruokun Yi ◽  
Yuxuan Wei ◽  
Fang Tan ◽  
Jianfei Mu ◽  
Xingyao Long ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Liver Injury ◽  
Oxidative Damage ◽  
Antioxidant Capacity ◽  
Camellia Sinensis ◽  
Interleukin 12 ◽  
Protective Effects ◽  
Oxide Synthase

Shoumei is a kind of white tea (slightly fermented Camellia sinensis) that is rich in polyphenols. In this study, polyphenols were extracted from Shoumei. High-performance liquid chromatography (HPLC) showed that the polyphenols included mainly gallic acid, catechin, hyperoside, and sulfuretin. In an in vitro experiment, H2O2 was used to induce oxidative damage in human normal hepatic L-02 cells. In an animal experiment, CCl4 was used to induce liver injury. The in vitro results showed that Shoumei polyphenols inhibited oxidative damage in normal hepatic L-02 cells, and the in vivo results showed that the polyphenols effectively reduced liver index values in mice with liver injury. The polyphenols also decreased aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), triglyceride (TG), total cholesterol (TC), blood urea nitrogen (BUN), nitric oxide (NO), malondialdehyde (MDA), interleukin 6 (IL-6), interleukin 12 (IL-12), tumour necrosis factor alpha (TNF-α), and interferon gamma (IFN-γ) levels and increased albumin (ALB), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) levels in the serum of mice with liver injury. Furthermore, pathological observation showed that the Shoumei polyphenols reduced CCl4-induced hepatocyte damage. qRT-PCR and Western blotting showed that the polyphenols upregulated the mRNA and protein expression of neuronal nitric oxide synthase (nNOS), endothelial nitric oxide synthase (eNOS), manganese- (Mn-) SOD, copper/zinc- (Cu/Zn-) SOD, CAT, and inhibitor of nuclear factor kappa B (NF-κB) alpha (IκB-α) and downregulated the expression of inducible nitric oxide synthase (iNOS) and NF-κB p65. The Shoumei polyphenols had a preventive effect against CCl4-induced mouse liver injury equivalent to that of silymarin. The four polyphenols identified as the key substances responsible for this effect mediated the effect through their antioxidant capacity. These results suggest that Shoumei polyphenols are high-quality natural products with liver-protective effects.

scholarly journals L-Carnitine has a liver-protective effect through inhibition of inducible nitric oxide synthase induction in primary cultured rat hepatocytes

2018 ◽  
Vol 8 (3) ◽  
pp. 212 ◽  
Author(s):  
Yusuke Nakamura ◽  
Hiroya Iida ◽  
Richi Nakatake ◽  
Tatsuma Sakaguchi ◽  
Masaki Kaibori ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Liver Injury ◽  
Inducible Nitric Oxide Synthase ◽  
Inos Mrna ◽  
Type I ◽  
Protective Effects ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Background: L-Carnitine has protective effects on various injured organs. However, it has not been reported whether L-carnitine influences the induction of inducible nitric oxide synthase (iNOS) expression during inflammation. Nitric oxide (NO) produced by iNOS is an inflammatory indicator in organs which become inflamed, including the liver.Objective: This study aimed to examine whether L-carnitine influences the induction of iNOS gene expression in inflammatory cytokine-stimulated hepatocytes and the mechanisms involved in the action. Methods: L-Carnitine was added into the primary cultures of rat hepatocytes stimulated by interleukin-1β (an in vitro liver injury model). The production of NO and induction of iNOS and its signaling pathway were analyzed.Results: Transfection experiments with iNOS promoter-luciferase constructs revealed how L-carnitine inhibited iNOS mRNA synthesis activity and reduced its stability. In support of this observation, L-carnitine reduced iNOS mRNA and iNOS protein expression levels, resulting in reduced NO production. L-Carnitine blocked two essential pathways for iNOS induction: IκB kinase (IκB degradation/NF-κB activation) and phosphatidylinositol 3-kinase/Akt (type I IL-1 receptor upregulation).Conclusions: L-Carnitine inhibited the induction of inflammatory mediator iNOS, partially through inhibition of NF-κB activation, which demonstrated L-carnitine has protective effects in an in vitro liver injury model. L-Carnitine may have therapeutic potential for organ injuries, including the liver.Keywords: L-carnitine, hepatic encephalopathy, inducible nitric oxide synthase, liver injury, primary cultured hepatocytes, nuclear factor-κB, type I interleukin-1 receptor 

scholarly journals Protective Effects of Millettia Pulchra Flavonoids on Myocardial Ischemia In Vitro and In Vivo

2015 ◽  
Vol 35 (2) ◽  
pp. 516-528 ◽  
Author(s):  
Jianchun Huang ◽  
Xudong Zhang ◽  
Feizhang Qin ◽  
Yingxin Li ◽  
Xiaoqun Duan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Myocardial Ischemia ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Protective Effects ◽  
Bax Protein ◽  
Oxide Synthase

Background: Previous studies have demonstrated that Millettia pulchra flavonoids (MPF) exhibit protective effects on myocardial ischemia reperfusion injury (MI/RI) in isolated rat hearts and show anti-oxidative, anti-hypoxic and anti-stress properties. Methods: In this study, the cardioprotective effects of MPF on myocardial ischemia and its underlying mechanisms were investigated by a hypoxia/ reoxygenation (H/R) injury model in vitro and a rat MI/RI model in vivo. Results: We found that the lactate dehydrogenase (LDH) and inducible nitric oxide synthase (iNOS) activities were decreased in the MPF pretreatment group, whereas the activities of constructional nitric oxide synthase (cNOS), total nitric oxide synthase (tNOS), Na+-K+-ATPase and Ca2+-Mg2+-ATPase were significantly increased. In addition, the cardiocytes were denser in the MPF groups than in the control group. The mortality rate and apoptosis rate of cardiocytes were significantly decreased. Furthermore, pretreatment with MPF in vivo significantly improved the hemodynamics, decreased malondialdehyde (MDA) abundance, increased the activities of plasma superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and decreased the expression of the Bax protein and ratio Bax/Bc1-2 ration. Conclusions: These results suggest that MPF is an attractive protective substance in myocardial ischemia due to its negative effects on heart rate and ionotropy, reduction of myocardial oxidative damage and modulation of gene expression associated with apoptosis.

scholarly journals Protective Effects of Caffeic Acid Phenethyl Ester (CAPE) and Novel Cape Analogue as Inducers of Heme Oxygenase-1 in Streptozotocin-Induced Type 1 Diabetic Rats

2019 ◽  
Vol 20 (10) ◽  
pp. 2441 ◽  
Author(s):  
Valeria Sorrenti ◽  
Marco Raffaele ◽  
Luca Vanella ◽  
Rosaria Acquaviva ◽  
Loredana Salerno ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Oxidative Damage ◽  
Caffeic Acid ◽  
Heme Oxygenase ◽  
Diabetic Rats ◽  
Heme Oxygenase 1 ◽  
Protective Effects ◽  
Oxide Synthase

Type 1 diabetes mellitus (T1D) is a chronic autoimmune disease resulting in the destruction of insulin producing β-cells of the pancreas, with consequent insulin deficiency and excessive glucose production. Hyperglycemia results in increased levels of reactive oxygen species (ROS) and nitrogen species (RNS) with consequent oxidative/nitrosative stress and tissue damage. Oxidative damage of the pancreatic tissue may contribute to endothelial dysfunction associated with diabetes. The aim of the present study was to investigate if the potentially protective effects of phenethyl ester of caffeic acid (CAPE), a natural phenolic compound occurring in a variety of plants and derived from honeybee hive propolis, and of a novel CAPE analogue, as heme oxygenase-1 (HO-1) inducers, could reduce pancreatic oxidative damage induced by excessive amount of glucose, affecting the nitric oxide synthase/dimethylarginine dimethylaminohydrolase (NOS/DDAH) pathway in streptozotocin-induced type 1 diabetic rats. Our data demonstrated that inducible nitric oxide synthase/gamma-Glutamyl-cysteine ligase (iNOS/GGCL) and DDAH dysregulation may play a key role in high glucose mediated oxidative stress, whereas HO-1 inducers such as CAPE or its more potent derivatives may be useful in diabetes and other stress-induced pathological conditions.

scholarly journals White Peony (Fermented Camellia sinensis) Polyphenols Help Prevent Alcoholic Liver Injury via Antioxidation

Antioxidants ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 524 ◽  
Author(s):  
Yalin Zhou ◽  
Fang Tan ◽  
Chong Li ◽  
Wenfeng Li ◽  
Wei Liao ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Nitric Oxide Synthase ◽  
Liver Injury ◽  
Camellia Sinensis ◽  
Quantitative Polymerase Chain Reaction ◽  
Radical Scavenging ◽  
Serum Levels ◽  
Alcoholic Liver Injury ◽  
Oxide Synthase

White peony is a type of white tea (Camellia sinensis) rich in polyphenols. In this study, polyphenols were extracted from white peony. In vitro experiments showed that white peony polyphenols (WPPs) possess strong free radical scavenging capabilities toward 2,2-Diphenyl-1-picrylhydrazyl (DPPH) and 2,2’-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS). Long-term alcohol gavage was used to induce alcoholic liver injury in mice, and relevant indices of liver injury were examined. WPPs effectively reduced the liver indices of mice with liver injury. The serum levels of aspartate aminotransferase (ATS), alanine aminotransferase (ALT), alkaline phosphatase (ALP), triglycerides (TG), total cholesterol (TC), blood urea nitrogen (BUN), nitric oxide (NO), and malondialdehyde (MDA) were downregulated, while those of albumin (ALB), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) were upregulated. WPPs also reduced the serum levels of interluekin-6 (IL-6), interluekin-12 (IL-12), tumor necrosis factor-alpha (TNF-α), and interferon-gamma (IFN-γ) in mice with liver injury. Pathology results showed that WPPs reduced alcohol-induced liver cell damage. Quantitative polymerase chain reaction (qPCR) and western blot results revealed that WPPs upregulated the mRNA and protein expressions of neuronal nitric oxide synthase (nNOS), endothelial nitric oxide synthase (eNOS), manganese superoxide dismutase (Mn-SOD), cupro–zinc superoxide dismutase (Cu/Zn-SOD), and CAT and downregulated iNOS expression in the liver of mice with liver injury. WPPs protected against alcoholic liver injury, and this effect was equivalent to that of silymarin. High-performance liquid chromatography revealed that WPPs mainly contained the polyphenols gallic acid, catechinic acid, and hyperoside, which are critical for exerting preventive effects against alcoholic liver injury. Thus, WPPs are high-quality natural products with liver protective effects.

scholarly journals Immune Suppression by Recombinant Interleukin (rIL)-12 Involves Interferon γ Induction of Nitric Oxide Synthase 2 (iNOS) Activity: Inhibitors of NO Generation Reveal the Extent of rIL-12 Vaccine Adjuvant Effect

1998 ◽  
Vol 188 (9) ◽  
pp. 1603-1610 ◽  
Author(s):  
Holly Kurzawa Koblish ◽  
Christopher A. Hunter ◽  
Maria Wysocka ◽  
Giorgio Trinchieri ◽  
William M.F. Lee
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Immune Suppression ◽  
Neutralizing Antibodies ◽  
Vaccine Adjuvant ◽  
Interleukin 12 ◽  
Effective Vaccine ◽  
Ifn Γ ◽  
Oxide Synthase

Recombinant interleukin 12 (IL-12) can profoundly suppress cellular immune responses in mice. To define the underlying mechanism, recombinant murine (rm)IL-12 was given to C57BL/6 mice undergoing alloimmunization and found to transiently but profoundly suppress in vivo and in vitro allogeneic responses and in vitro splenocyte mitogenic responses. Use of neutralizing antibodies and genetically deficient mice showed that IFN-γ (but not TNF-α) mediated rmIL-12–induced immune suppression. Splenocyte fractionation studies revealed that adherent cells from rmIL-12–treated mice suppressed the mitogenic response of normal nonadherent cells to concanavalin A and IL-2. Addition of an inhibitor of nitric oxide synthase (NOS) restored mitogenic responses, and inducible (i)NOS−/− mice were not immunosuppressed by rmIL-12. These results support the view that suppression of T cell responses is due to NO produced by macrophages responding to the high levels of IFN-γ induced by rmIL-12. When a NOS inhibitor was given with rmIL-12 during vaccination of A/J mice with irradiated SCK tumor cells, immunosuppression was averted and the extent of rmIL-12's ability to enhance induction of protective antitumor immunity was revealed. This demonstrates that rmIL-12 is an effective vaccine adjuvant whose efficacy may be masked by its transient immunosuppressive effect.

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