Role of the Phytochemical Compounds like Modulators in Gut Microbiota and Oxidative Stress

Background: Currently, daily consumption of green herb functional food or medicinal herbs has increased as adopted by many people worldwide as a way of life or even as an alternative to the use of synthetic medicines. Phytochemicals, which are a series of compounds of relatively complex structures and restricted distribution in plants, usually perform the defensive functions for plants against insects, bacteria, fungi or other pathogenic factors. A series of studies have found their effectiveness in the treatment or prevention of systemic diseases such as autoimmune diseases, cancer, neurodegenerative diseases, Crohn's disease and so on. Objective: This review systematizes the literature on the mechanisms of the phytochemicals that react against unique free radicals and prevent the oxidative stress and also summarizes their role in gut microbiota inhibiting bacterial translocation and damage to the intestinal barrier and improving the intestinal membrane condition. Conclusion: The gut microbiota modulation and antioxidant activities of the phytochemicals shall be emphasized on the research of the active principles of the phytochemicals.

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Gut microbiota accelerates cisplatin-induced acute liver injury associated with robust inflammation and oxidative stress in mice

Journal of Translational Medicine ◽

10.1186/s12967-021-02814-5 ◽

2021 ◽

Vol 19 (1) ◽

Author(s):

Shenhai Gong ◽

Yinglin Feng ◽

Yunong Zeng ◽

Huanrui Zhang ◽

Meiping Pan ◽

...

Keyword(s):

Oxidative Stress ◽

16S Rrna ◽

Gut Microbiota ◽

Gene Sequencing ◽

16S Rrna Gene Sequencing ◽

Rrna Gene ◽

Metabolomic Analysis ◽

Rrna Gene Sequencing ◽

And Oxidative Stress

Abstract Background Gut microbiota has been reported to be disrupted by cisplatin, as well as to modulate chemotherapy toxicity. However, the precise role of intestinal microbiota in the pathogenesis of cisplatin hepatotoxicity remains unknown. Methods We compared the composition and function of gut microbiota between mice treated with and without cisplatin using 16S rRNA gene sequencing and via metabolomic analysis. For understanding the causative relationship between gut dysbiosis and cisplatin hepatotoxicity, antibiotics were administered to deplete gut microbiota and faecal microbiota transplantation (FMT) was performed before cisplatin treatment. Results 16S rRNA gene sequencing and metabolomic analysis showed that cisplatin administration caused gut microbiota dysbiosis in mice. Gut microbiota ablation by antibiotic exposure protected against the hepatotoxicity induced by cisplatin. Interestingly, mice treated with antibiotics dampened the mitogen-activated protein kinase pathway activation and promoted nuclear factor erythroid 2-related factor 2 nuclear translocation, resulting in decreased levels of both inflammation and oxidative stress in the liver. FMT also confirmed the role of microbiota in individual susceptibility to cisplatin-induced hepatotoxicity. Conclusions This study elucidated the mechanism by which gut microbiota mediates cisplatin hepatotoxicity through enhanced inflammatory response and oxidative stress. This knowledge may help develop novel therapeutic approaches that involve targeting the composition and metabolites of microbiota.

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Protective Role of Natural and Semi-Synthetic Tocopherols on TNFα-Induced ROS Production and ICAM-1 and Cl-2 Expression in HT29 Intestinal Epithelial Cells

Antioxidants ◽

10.3390/antiox10020160 ◽

2021 ◽

Vol 10 (2) ◽

pp. 160

Author(s):

Vladana Domazetovic ◽

Irene Falsetti ◽

Caterina Viglianisi ◽

Kristian Vasa ◽

Cinzia Aurilia ◽

...

Keyword(s):

Oxidative Stress ◽

Antioxidant Properties ◽

Intestinal Barrier ◽

Protective Role ◽

Intercellular Adhesion Molecule ◽

Intestinal Epithelial ◽

Intercellular Adhesion Molecule 1 ◽

Beneficial Effects ◽

Bowel Diseases

Vitamin E, a fat-soluble compound, possesses both antioxidant and non-antioxidant properties. In this study we evaluated, in intestinal HT29 cells, the role of natural tocopherols, α-Toc and δ-Toc, and two semi-synthetic derivatives, namely bis-δ-Toc sulfide (δ-Toc)2S and bis-δ-Toc disulfide (δ-Toc)2S2, on TNFα-induced oxidative stress, and intercellular adhesion molecule-1 (ICAM-1) and claudin-2 (Cl-2) expression. The role of tocopherols was compared to that of N-acetylcysteine (NAC), an antioxidant precursor of glutathione synthesis. The results show that all tocopherol containing derivatives used, prevented TNFα-induced oxidative stress and the increase of ICAM-1 and Cl-2 expression, and that (δ-Toc)2S and (δ-Toc)2S2 are more effective than δ-Toc and α-Toc. The beneficial effects demonstrated were due to tocopherol antioxidant properties, but suppression of TNFα-induced Cl-2 expression seems not only to be related with antioxidant ability. Indeed, while ICAM-1 expression is strongly related to the intracellular redox state, Cl-2 expression is TNFα-up-regulated by both redox and non-redox dependent mechanisms. Since ICAM-1 and Cl-2 increase intestinal bowel diseases, and cause excessive recruitment of immune cells and alteration of the intestinal barrier, natural and, above all, semi-synthetic tocopherols may have a potential role as a therapeutic support against intestinal chronic inflammation, in which TNFα represents an important proinflammatory mediator.

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Insights into the Impact of Microbiota in the Treatment of NAFLD/NASH and Its Potential as a Biomarker for Prognosis and Diagnosis

Biomedicines ◽

10.3390/biomedicines9020145 ◽

2021 ◽

Vol 9 (2) ◽

pp. 145

Author(s):

Julio Plaza-Díaz ◽

Patricio Solis-Urra ◽

Jerónimo Aragón-Vela ◽

Fernando Rodríguez-Rodríguez ◽

Jorge Olivares-Arancibia ◽

...

Keyword(s):

Gut Microbiota ◽

Fecal Microbiota Transplantation ◽

Liver Steatosis ◽

Intestinal Barrier ◽

Fecal Microbiota ◽

Current Treatment ◽

Immune Defense ◽

Alcoholic Fatty Liver ◽

The Impact

Non-alcoholic fatty liver disease (NAFLD) is an increasing cause of chronic liver illness associated with obesity and metabolic disorders, such as hypertension, dyslipidemia, or type 2 diabetes mellitus. A more severe type of NAFLD, non-alcoholic steatohepatitis (NASH), is considered an ongoing global health threat and dramatically increases the risks of cirrhosis, liver failure, and hepatocellular carcinoma. Several reports have demonstrated that liver steatosis is associated with the elevation of certain clinical and biochemical markers but with low predictive potential. In addition, current imaging methods are inaccurate and inadequate for quantification of liver steatosis and do not distinguish clearly between the microvesicular and the macrovesicular types. On the other hand, an unhealthy status usually presents an altered gut microbiota, associated with the loss of its functions. Indeed, NAFLD pathophysiology has been linked to lower microbial diversity and a weakened intestinal barrier, exposing the host to bacterial components and stimulating pathways of immune defense and inflammation via toll-like receptor signaling. Moreover, this activation of inflammation in hepatocytes induces progression from simple steatosis to NASH. In the present review, we aim to: (a) summarize studies on both human and animals addressed to determine the impact of alterations in gut microbiota in NASH; (b) evaluate the potential role of such alterations as biomarkers for prognosis and diagnosis of this disorder; and (c) discuss the involvement of microbiota in the current treatment for NAFLD/NASH (i.e., bariatric surgery, physical exercise and lifestyle, diet, probiotics and prebiotics, and fecal microbiota transplantation).

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The DNA Sensor AIM2 Protects against Streptozotocin-Induced Type 1 Diabetes by Regulating Intestinal Homeostasis via the IL-18 Pathway

Cells ◽

10.3390/cells9040959 ◽

2020 ◽

Vol 9 (4) ◽

pp. 959 ◽

Cited By ~ 2

Author(s):

Jefferson Antônio Leite ◽

Gabriela Pessenda ◽

Isabel C. Guerra-Gomes ◽

Alynne Karen Mendonça de Santana ◽

Camila André Pereira ◽

...

Keyword(s):

Type 1 Diabetes ◽

Gut Microbiota ◽

Bacterial Translocation ◽

Intestinal Barrier ◽

Intestinal Barrier Function ◽

Dna Sensor ◽

Proinflammatory Response

Pattern recognition receptors (PRRs), such as Nod2, Nlrp3, Tlr2, Trl4, and Tlr9, are directly involved in type 1 diabetes (T1D) susceptibility. However, the role of the cytosolic DNA sensor, AIM2, in T1D pathogenesis is still unknown. Here, we demonstrate that C57BL/6 mice lacking AIM2 (AIM2−/−) are prone to streptozotocin (STZ)-induced T1D, compared to WT C57BL/6 mice. The AIM2−/− mice phenotype is associated with a greater proinflammatory response in pancreatic tissues, alterations in gut microbiota and bacterial translocation to pancreatic lymph nodes (PLNs). These alterations are related to an increased intestinal permeability mediated by tight-junction disruption. Notably, AIM2−/− mice treated with broad-spectrum antibiotics (ABX) are protected from STZ-induced T1D and display a lower pancreatic proinflammatory response. Mechanistically, the AIM2 inflammasome is activated in vivo, leading to an IL-18 release in the ileum at 15 days after an STZ injection. IL-18 favors RegIIIγ production, thus mitigating gut microbiota alterations and reinforcing the intestinal barrier function. Together, our findings show a regulatory role of AIM2, mediated by IL-18, in shaping gut microbiota and reducing bacterial translocation and proinflammatory response against insulin-producing β cells, which ultimately results in protection against T1D onset in an STZ-induced diabetes model.

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Bioactives and their metabolites from Tetrastigma hemsleyanum leaves ameliorate DSS-induced colitis via protecting intestinal barrier, mitigating oxidative stress and regulating gut microbiota

Food & Function ◽

10.1039/d1fo02588k ◽

2021 ◽

Author(s):

Tong Wu ◽

Xiaoya Wang ◽

Hua Xiong ◽

Zeyuan Deng ◽

Xin Peng ◽

...

Keyword(s):

Oxidative Stress ◽

Medicinal Plant ◽

Gut Microbiota ◽

Intestinal Barrier ◽

Tetrastigma Hemsleyanum ◽

Research Attention

Tetrastigma hemsleyanum, a precious edible and medicinal plant in China, has attracted extensive research attention in recent years due to its highly traditional value for the treatment of various diseases....

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ROLE OF THE GENETIC FACTORS, DETOXICATION SYSTEMS AND OXIDATIVE STRESS IN THE PATHOGENESIS OF ENDOMETRIOSIS AND INFERTILITY (REVIEW)

Annals of the Russian academy of medical sciences ◽

10.15690/vramn.v68i8.717 ◽

2013 ◽

Vol 68 (8) ◽

pp. 14-19 ◽

Cited By ~ 4

Author(s):

E. D. Dubinskaya ◽

A. S. Gasparov ◽

T. A. Fedorova ◽

N. V. Lapteva

Keyword(s):

Oxidative Stress ◽

Genetic Factors ◽

Antioxidant Activities ◽

Polycystic Ovary ◽

Reproductive Function ◽

Detoxification Enzyme ◽

Systemic Oxidative Stress ◽

Exogenous Factors ◽

And Oxidative Stress

The aim of this paper is to provide a systematic review of the role of the genetic factors, detoxication systems and oxidative stress in the pathogenesis of endometriosis and infertility. Endometriosis and infertility are still both the most uncommon diseases in gynecology. Many aspects of female reproductive function are strongly influenced by genetic factors, and numerous studies have attempted to identify susceptibility genes for disorders affecting female fertility such as polycystic ovary syndrome, endometriosis, fibroids, cancer (ovarian, vulvar, cervical), premature ovarian failure, recurrent pregnancy loss and pre-eclampsia. The most solid evidence linking specific polymorphisms to endometriosis is showed by the studies investigating a phase II detoxification enzyme. No data were found concerning influences of the genetic factors on the female infertility. Contrary, a lot of studies devoted to the genetic factors of male infertility are presented. It’s known that endometriosis associated with increased systemic oxidative stress. The implication of increased systemic oxidative stress in disease progression or the association with other oxidative stress-related pathologic conditions needs to be addressed in further studies. The majority of studies suggest a reduced antioxidant capacity in infertile women with endometriosis. In the present review we discussed the role of the genetic factors in the pathogenesis of endometriosis and infertility. NAT2 polimorphism, xenobiotic methabolism and exogenous factors are somehow related with these diseases. An altered balance between pro-oxidant and antioxidant activities may have an impact on folliculogenesis and adequate embryo development.

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The Role of Gut Microbiota in Intestinal Inflammation with Respect to Diet and Extrinsic Stressors

Microorganisms ◽

10.3390/microorganisms7080271 ◽

2019 ◽

Vol 7 (8) ◽

pp. 271 ◽

Cited By ~ 26

Author(s):

Stefani Lobionda ◽

Panida Sittipo ◽

Hyog Young Kwon ◽

Yun Kyung Lee

Keyword(s):

Gut Microbiota ◽

Intestinal Inflammation ◽

Intestinal Barrier ◽

Environmental Stressors ◽

Intestinal Barrier Function ◽

Symbiotic Relationship ◽

Inflammatory Bowel ◽

Host Metabolism ◽

The Relationship

The gut microbiota maintains a symbiotic relationship with the host and regulates several important functions including host metabolism, immunity, and intestinal barrier function. Intestinal inflammation and inflammatory bowel disease (IBD) are commonly associated with dysbiosis of the gut microbiota. Alterations in the gut microbiota and associated changes in metabolites as well as disruptions in the intestinal barrier are evidence of the relationship between the gut microbiota and intestinal inflammation. Recent studies have found that many factors may alter the gut microbiota, with the effects of diet being commonly-studied. Extrinsic stressors, including environmental stressors, antibiotic exposure, sleep disturbance, physical activity, and psychological stress, may also play important roles in altering the composition of the gut microbiota. Herein, we discuss the roles of the gut microbiota in intestinal inflammation in relation to diet and other extrinsic stressors.

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Gut Microbiota in Alzheimer’s Disease, Depression, and Type 2 Diabetes Mellitus: The Role of Oxidative Stress

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/4730539 ◽

2019 ◽

Vol 2019 ◽

pp. 1-10 ◽

Cited By ~ 11

Author(s):

Maria Luca ◽

Maurizio Di Mauro ◽

Marco Di Mauro ◽

Antonina Luca

Keyword(s):

Oxidative Stress ◽

Diabetes Mellitus ◽

Alzheimer’S Disease ◽

Type 2 Diabetes ◽

Alzheimer's Disease ◽

Type 2 Diabetes Mellitus ◽

Gut Microbiota ◽

Therapeutic Implications

Gut microbiota consists of over 100 trillion microorganisms including at least 1000 different species of bacteria and is crucially involved in physiological and pathophysiological processes occurring in the host. An imbalanced gastrointestinal ecosystem (dysbiosis) seems to be a contributor to the development and maintenance of several diseases, such as Alzheimer’s disease, depression, and type 2 diabetes mellitus. Interestingly, the three disorders are frequently associated as demonstrated by the high comorbidity rates. In this review, we introduce gut microbiota and its role in both normal and pathological processes; then, we discuss the importance of the gut-brain axis as well as the role of oxidative stress and inflammation as mediators of the pathological processes in which dysbiosis is involved. Specific sections pertain the role of the altered gut microbiota in the pathogenesis of Alzheimer’s disease, depression, and type 2 diabetes mellitus. The therapeutic implications of microbiota manipulation are briefly discussed. Finally, a conclusion comments on the possible role of dysbiosis as a common pathogenetic contributor (via oxidative stress and inflammation) shared by the three disorders.

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Role of Gut Microbiota in Multiple Sclerosis and Potential Therapeutic Implications

Current Neuropharmacology ◽

10.2174/1570159x19666210629145351 ◽

2021 ◽

Vol 19 ◽

Author(s):

Xu Wang ◽

Zhen Liang ◽

Shengnan Wang ◽

Di Ma ◽

Mingqin Zhu ◽

...

Keyword(s):

Multiple Sclerosis ◽

Gut Microbiota ◽

Demyelinating Disease ◽

Inflammatory Diseases ◽

Intestinal Barrier ◽

Autoimmune Response ◽

Therapeutic Implications ◽

The Central Nervous System ◽

Underlying Mechanisms

: The role of gut microbiota in health and diseases has been receiving increased attention recently. Emerging evidence from previous studies on the gut-microbiota-brain axis highlighted the importance of gut microbiota in neurological disorders. Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating disease of the central nervous system (CNS) resulting from T-cell-driven, myelin-directed autoimmunity. The dysbiosis of gut microbiota in MS patients has been reported in published research studies, indicating that gut microbiota plays an important role in the pathogenesis of MS. Gut microbiota has also been reported to influence the initiation of disease and severity of experimental autoimmune encephalomyelitis, which is the animal model of MS. However, the underlying mechanisms of gut microbiota involvement in the pathogenesis of MS remain unclear. Therefore, in this review, we summerized the potential mechanisms for gut microbiota involvement in the pathogenesis of MS, including increasing the permeability of the intestinal barrier, initiating an autoimmune response, disrupting the blood-brain barrier integrity, and contributing to chronic inflammation. The possibility for gut microbiota as a target for MS therapy has also been discussed. This review provides new insight into understanding the role of gut microbiota in neurological and inflammatory diseases.

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