Insights into the Role and Interdependence of Oxidative Stress and Inflammation in Liver Diseases

The crucial roles of oxidative stress and inflammation in the development of hepatic diseases have been unraveled and emphasized for decades. From steatosis to fibrosis, cirrhosis and liver cancer, hepatic oxidative stress, and inflammation are sustained and participated in this pathological progressive process. Notably, increasing evidences showed that oxidative stress and inflammation are tightly related, which are regarded as essential partners that present simultaneously and interact with each other in various pathological conditions, creating a vicious cycle to aggravate the hepatic diseases. Clarifying the interaction of oxidative stress and inflammation is of great importance to provide new directions and targets for developing therapeutic intervention. Herein, this review is concerned with the regulation and interdependence of oxidative stress and inflammation in a variety of liver diseases. In addition to classical mediators and signaling, particular emphasis is placed upon immune suppression, a potential linkage of oxidative stress and inflammation, to provide new inspiration for the treatment of liver diseases. Furthermore, since antioxidation and anti-inflammation have been extensively attempted as the strategies for treatment of liver diseases, the application of herbal medicines and their derived compounds that protect liver from injury via regulating oxidative stress and inflammation collectively were reviewed and discussed.

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Assessment of miR-212 and Other Biomarkers in the Diagnosis and Treatment of HBV-infection-related Liver Diseases

Current Drug Metabolism ◽

10.2174/1389200220666191011120434 ◽

2019 ◽

Vol 20 (10) ◽

pp. 785-798 ◽

Cited By ~ 1

Author(s):

Yigan Zhang ◽

Huaze Xi ◽

Xin Nie ◽

Peng Zhang ◽

Ning Lan ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Chronic Hepatitis ◽

Liver Cancer ◽

Hepatitis B ◽

Chronic Hepatitis B ◽

Liver Diseases ◽

Meld Score ◽

Hbv Infection ◽

Expression Level ◽

Control Group

Objective: Our study aims to detect the sensitivity of the new biomarker miR-212 existing in serum exosomes along with other hepatocellular carcinoma biomarkers such as AFP (alpha-fetoprotein), CA125 (carbohydrate antigen-ca125), and Hbx protein in the diagnosis of HBV-related liver diseases. We also aim to study the roles of these biomarkers in the progression of chronic hepatitis B and provide scientific data to show the clinical value of these biomarkers. Methods: We selected 200 patients with HBV-infection (58 cases of chronic hepatitis B, 47 cases of hepatocellular carcinoma, 30 cases of compensatory phase cirrhosis, and 65 cases of decompensatory phase cirrhosis), 31 patients with primary liver cancer without HBV infection, and 70 healthy individuals as the control group. The expression level of serum AFP and CA125 was detected with electrochemiluminescence immunoassay. The expression level of the Hbx protein was detected with ELISA. Meanwhile, the expression level of miR-212 in serum was analyzed with RT-qPCR. We collected patients’ clinical information following the Child-Pugh classification and MELD score criterion, and statistical analysis was made between the expression level of miR-212 and the collected clinical indexes. Lastly, we predicted the target genes of the miR-212 and its functions using bioinformatics methods such as cluster analysis and survival prediction. Results: Compared to the control group, the expression level of miR-212 in HBV infected patients was remarkably increased (P<0.05), especially between the HBV-infection Hepatocellular carcinoma group and the non-HBVinfection liver cancer group (P<0.05). The expression of miR-212 was increased in patients’ Child-Pugh classification, MELD score, and TNM staging. Moreover, the sensitivity and specificity of miR-212 were superior to AFP, CA125, and HBx protein. Conclusion: There is a linear relationship between disease progression and expression level of miR-212 in the serum of HBV infected patients. This demonstrates that miR-212 plays a significant role in liver diseases. miR-212 is expected to be a new biomarker used for the diagnosis and assessment of patients with HBV-infection-related liver diseases.

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Salidroside from Rhodiola rosea L. attenuates diabetic nephropathy in STZ induced diabetic rats via anti-oxidative stress, anti-inflammation, and inhibiting TGF-β1/Smad pathway

Journal of Functional Foods ◽

10.1016/j.jff.2020.104329 ◽

2021 ◽

Vol 77 ◽

pp. 104329

Author(s):

Shan Shan Qi ◽

Meng Li Shao ◽

Sun Ze ◽

Hong Xing Zheng

Keyword(s):

Oxidative Stress ◽

Diabetic Nephropathy ◽

Diabetic Rats ◽

Rhodiola Rosea ◽

Smad Pathway ◽

Anti Inflammation ◽

Tgf Β1

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The Contribution of Microglia to Neuroinflammation in Parkinson’s Disease

International Journal of Molecular Sciences ◽

10.3390/ijms22094676 ◽

2021 ◽

Vol 22 (9) ◽

pp. 4676

Author(s):

Katja Badanjak ◽

Sonja Fixemer ◽

Semra Smajić ◽

Alexander Skupin ◽

Anne Grünewald

Keyword(s):

Oxidative Stress ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Inflammatory Cytokine ◽

Population Ageing ◽

Future Research ◽

Cytokine Release ◽

Vicious Cycle ◽

Inflammatory Processes ◽

Great Evidence

With the world’s population ageing, the incidence of Parkinson’s disease (PD) is on the rise. In recent years, inflammatory processes have emerged as prominent contributors to the pathology of PD. There is great evidence that microglia have a significant neuroprotective role, and that impaired and over activated microglial phenotypes are present in brains of PD patients. Thereby, PD progression is potentially driven by a vicious cycle between dying neurons and microglia through the instigation of oxidative stress, mitophagy and autophagy dysfunctions, a-synuclein accumulation, and pro-inflammatory cytokine release. Hence, investigating the involvement of microglia is of great importance for future research and treatment of PD. The purpose of this review is to highlight recent findings concerning the microglia-neuronal interplay in PD with a focus on human postmortem immunohistochemistry and single-cell studies, their relation to animal and iPSC-derived models, newly emerging technologies, and the resulting potential of new anti-inflammatory therapies for PD.

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Heme Oxygenase-1 Induction by Cobalt Protoporphyrin Ameliorates Cholestatic Liver Disease in a Xenobiotic-Induced Murine Model

International Journal of Molecular Sciences ◽

10.3390/ijms22158253 ◽

2021 ◽

Vol 22 (15) ◽

pp. 8253

Author(s):

Jung-Yeon Kim ◽

Yongmin Choi ◽

Jaechan Leem ◽

Jeong Eun Song

Keyword(s):

Oxidative Stress ◽

Liver Disease ◽

Heme Oxygenase ◽

Murine Model ◽

Liver Diseases ◽

Transforming Growth Factor ◽

Heme Oxygenase 1 ◽

Cholestatic Liver Disease ◽

Hepatocyte Apoptosis ◽

Cobalt Protoporphyrin

Cholestatic liver diseases can progress to end-stage liver disease and reduce patients’ quality of life. Although their underlying mechanisms are still incompletely elucidated, oxidative stress is considered to be a key contributor to these diseases. Heme oxygenase-1 (HO-1) is a cytoprotective enzyme that displays antioxidant action. It has been found that this enzyme plays a protective role against various inflammatory diseases. However, the role of HO-1 in cholestatic liver diseases has not yet been investigated. Here, we examined whether pharmacological induction of HO-1 by cobalt protoporphyrin (CoPP) ameliorates cholestatic liver injury. To this end, a murine model of 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet feeding was used. Administration of CoPP ameliorated liver damage and cholestasis with HO-1 upregulation in DDC diet-fed mice. Induction of HO-1 by CoPP suppressed the DDC diet-induced oxidative stress and hepatocyte apoptosis. In addition, CoPP attenuated cytokine production and inflammatory cell infiltration. Furthermore, deposition of the extracellular matrix and expression of fibrosis-related genes after DDC feeding were also decreased by CoPP. HO-1 induction decreased the number of myofibroblasts and inhibited the transforming growth factor-β pathway. Altogether, these data suggest that the pharmacological induction of HO-1 ameliorates cholestatic liver disease by suppressing oxidative stress, hepatocyte apoptosis, and inflammation.

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A polysaccharide of PFP-1 from Pleurotus geesteranus attenuates alcoholic liver diseases via Nrf2 and NF-κB signaling pathways

Food & Function ◽

10.1039/d1fo00310k ◽

2021 ◽

Author(s):

Xinling Song ◽

Wenxue Sun ◽

Wenxin Cai ◽

Le Jia ◽

Jianjun Zhang

Keyword(s):

Oxidative Stress ◽

Liver Disease ◽

Liver Injury ◽

Signaling Pathways ◽

Alcoholic Liver Disease ◽

Fruiting Body ◽

Liver Diseases ◽

Alcoholic Liver Diseases

A polysaccharide named as PFP-1 was isolated from Pleurotus geesteranus fruiting body, and the potential investigations on ameliorating oxidative stress and liver injury against alcoholic liver disease (ALD) were processed...

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Nanomaterials and hepatic disease: toxicokinetics, disease types, intrinsic mechanisms, liver susceptibility, and influencing factors

Journal of Nanobiotechnology ◽

10.1186/s12951-021-00843-2 ◽

2021 ◽

Vol 19 (1) ◽

Author(s):

Ting Sun ◽

Yiyuan Kang ◽

Jia Liu ◽

Yanli Zhang ◽

Lingling Ou ◽

...

Keyword(s):

Liver Disease ◽

Liver Cancer ◽

Metabolic Disorders ◽

Hepatic Disease ◽

Target Organ ◽

Hepatic Diseases ◽

Toxicological Studies ◽

Main Target ◽

Potential Risks ◽

Further Development

AbstractThe widespread use of nanomaterials (NMs) has raised concerns that exposure to them may introduce potential risks to the human body and environment. The liver is the main target organ for NMs. Hepatotoxic effects caused by NMs have been observed in recent studies but have not been linked to liver disease, and the intrinsic mechanisms are poorly elucidated. Additionally, NMs exhibit varied toxicokinetics and induce enhanced toxic effects in susceptible livers; however, thus far, this issue has not been thoroughly reviewed. This review provides an overview of the toxicokinetics of NMs. We highlight the possibility that NMs induce hepatic diseases, including nonalcoholic steatohepatitis (NASH), fibrosis, liver cancer, and metabolic disorders, and explore the underlying intrinsic mechanisms. Additionally, NM toxicokinetics and the potential induced risks in the livers of susceptible individuals, including subjects with liver disease, obese individuals, aging individuals and individuals of both sexes, are summarized. To understand how NM type affect their toxicity, the influences of the physicochemical and morphological (PCM) properties of NMs on their toxicokinetics and toxicity are also explored. This review provides guidance for further toxicological studies on NMs and will be important for the further development of NMs for applications in various fields.

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Apigenin protects mice against 3,5-diethoxycarbonyl-1,4-dihydrocollidine-induced cholestasis

Food & Function ◽

10.1039/d0fo02910f ◽

2021 ◽

Vol 12 (5) ◽

pp. 2323-2334

Author(s):

Shihong Zheng ◽

Peichang Cao ◽

Zequn Yin ◽

Xuerui Wang ◽

Yuanli Chen ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Metabolism ◽

Liver Fibrosis ◽

Liver Damage ◽

Liver Diseases ◽

Potential Drug ◽

Abnormal Lipid Metabolism ◽

And Oxidative Stress

Apigenin prevented the DDC-induced abnormal lipid metabolism, liver damage and liver fibrosis by reducing inflammation and oxidative stress. Apigenin might be a potential drug for the treatment of cholestatic liver diseases.

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Silver nanoparticles mitigate Aeromonas hydrophila-induced immune suppression, oxidative stress, and apoptotic and genotoxic effects in Oreochromis niloticus

Aquaculture ◽

10.1016/j.aquaculture.2021.736430 ◽

2021 ◽

Vol 535 ◽

pp. 736430

Author(s):

Walaa El-Houseiny ◽

Mohamed Fouad Mansour ◽

Wafaa A.M. Mohamed ◽

Naif A. Al-Gabri ◽

Ahmed A. El-Sayed ◽

...

Keyword(s):

Oxidative Stress ◽

Silver Nanoparticles ◽

Immune Suppression ◽

Aeromonas Hydrophila ◽

Oreochromis Niloticus ◽

Genotoxic Effects

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Green Tea and Epigallocatechin Gallate (EGCG) for the Management of Nonalcoholic Fatty Liver Diseases (NAFLD): Insights into the Role of Oxidative Stress and Antioxidant Mechanism

Antioxidants ◽

10.3390/antiox10071076 ◽

2021 ◽

Vol 10 (7) ◽

pp. 1076

Author(s):

Guoyi Tang ◽

Yu Xu ◽

Cheng Zhang ◽

Ning Wang ◽

Huabin Li ◽

...

Keyword(s):

Oxidative Stress ◽

Fatty Liver ◽

Green Tea ◽

Liver Diseases ◽

Randomized Clinical Trials ◽

Epigallocatechin Gallate ◽

Protective Effects ◽

Nonalcoholic Fatty Liver ◽

Nonalcoholic Fatty Liver Diseases ◽

Underlying Mechanisms

Nonalcoholic fatty liver diseases (NAFLD) represent a set of liver disorders progressing from steatosis to steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma, which induce huge burden to human health. Many pathophysiological factors are considered to influence NAFLD in a parallel pattern, involving insulin resistance, oxidative stress, lipotoxicity, mitochondrial dysfunction, endoplasmic reticulum stress, inflammatory cascades, fibrogenic reaction, etc. However, the underlying mechanisms, including those that induce NAFLD development, have not been fully understood. Specifically, oxidative stress, mainly mediated by excessive accumulation of reactive oxygen species, has participated in the multiple NAFLD-related signaling by serving as an accelerator. Ameliorating oxidative stress and maintaining redox homeostasis may be a promising approach for the management of NAFLD. Green tea is one of the most important dietary resources of natural antioxidants, above which epigallocatechin gallate (EGCG) notably contributes to its antioxidative action. Accumulative evidence from randomized clinical trials, systematic reviews, and meta-analysis has revealed the beneficial functions of green tea and EGCG in preventing and managing NAFLD, with acceptable safety in the patients. Abundant animal and cellular studies have demonstrated that green tea and EGCG may protect against NAFLD initiation and development by alleviating oxidative stress and the related metabolism dysfunction, inflammation, fibrosis, and tumorigenesis. The targeted signaling pathways may include, but are not limited to, NRF2, AMPK, SIRT1, NF-κB, TLR4/MYD88, TGF-β/SMAD, and PI3K/Akt/FoxO1, etc. In this review, we thoroughly discuss the oxidative stress-related mechanisms involved in NAFLD development, as well as summarize the protective effects and underlying mechanisms of green tea and EGCG against NAFLD.

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