Systemic epigallocatechin gallate protects against retinal degeneration and hepatic oxidative stress in the P23H-1 rat

Background: Retinitis pigmentosa (RP) is a group of inherited retinal dystrophies characterized by progressive degeneration of photoreceptor cells. Ocular redox status is altered in RP suggesting oxidative stress could contribute to their progression. In this study, we investigated the effect of a mixture of nutraceuticals with antioxidant properties (NUT) on retinal degeneration in rd10 mice, a model of RP. Methods: NUT was orally administered to rd10 mice from postnatal day (PD) 9 to PD18. At PD18 retinal function and morphology were examined by electroretinography (ERG) and histology including TUNEL assay, immunolabeling of microglia, Müller cells, and poly ADP ribose polymers. Retinal redox status was determined by measuring the activity of antioxidant enzymes and some oxidative stress markers. Gene expression of the cytokines IL-6, TNFα, and IL-1β was assessed by real-time PCR. Results: NUT treatment delayed the loss of photoreceptors in rd10 mice partially preserving their electrical responses to light stimuli. Moreover, it ameliorated redox status and reduced inflammation including microglia activation, upregulation of cytokines, reactive gliosis, and PARP overactivation. Conclusions: NUT ameliorated retinal functionality and morphology at early stages of RP in rd10 mice. This formulation could be useful as a neuroprotective approach for patients with RP in the future.

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Protective effect of Rumex patientia (English Spinach) roots on ferric nitrilotriacetate (Fe-NTA) induced hepatic oxidative stress and tumor promotion response

Food and Chemical Toxicology ◽

10.1016/j.fct.2007.03.021 ◽

2007 ◽

Vol 45 (10) ◽

pp. 1821-1829 ◽

Cited By ~ 14

Author(s):

Irshad A. Lone ◽

Gurpreet Kaur ◽

Mohammad Athar ◽

M. Sarwar Alam

Keyword(s):

Oxidative Stress ◽

Protective Effect ◽

Tumor Promotion ◽

Ferric Nitrilotriacetate ◽

Hepatic Oxidative Stress

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Vitamin D deficiency exacerbates hepatic oxidative stress and inflammation during acetaminophen-induced acute liver injury in mice

International Immunopharmacology ◽

10.1016/j.intimp.2021.107716 ◽

2021 ◽

Vol 97 ◽

pp. 107716

Author(s):

Ya-Qi Wang ◽

Xiao-Pan Geng ◽

Ming-Wei Wang ◽

Hong-Qian Wang ◽

Cheng Zhang ◽

...

Keyword(s):

Oxidative Stress ◽

Vitamin D ◽

Liver Injury ◽

Vitamin D Deficiency ◽

Acute Liver Injury ◽

Hepatic Oxidative Stress

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Oxidative Stress Mediates the Fetal Programming of Hypertension by Glucocorticoids

Antioxidants ◽

10.3390/antiox10040531 ◽

2021 ◽

Vol 10 (4) ◽

pp. 531

Author(s):

Jeremy Lamothe ◽

Sandhya Khurana ◽

Sujeenthar Tharmalingam ◽

Chad Williamson ◽

Collin J. Byrne ◽

...

Keyword(s):

Oxidative Stress ◽

Blood Pressure ◽

Superoxide Dismutase ◽

Fetal Programming ◽

Cardiovascular Health ◽

Phenylalanine Hydroxylase ◽

Epigallocatechin Gallate ◽

Female Offspring ◽

Glutathione Peroxidase 1 ◽

Protein Levels

The field of cardiovascular fetal programming has emphasized the importance of the uterine environment on postnatal cardiovascular health. Studies have linked increased fetal glucocorticoid exposure, either from exogenous sources (such as dexamethasone (Dex) injections), or from maternal stress, to the development of adult cardiovascular pathologies. Although the mechanisms are not fully understood, alterations in gene expression driven by altered oxidative stress and epigenetic pathways are implicated in glucocorticoid-mediated cardiovascular programming. Antioxidants, such as the naturally occurring polyphenol epigallocatechin gallate (EGCG), or the superoxide dismutase (SOD) 4-hydroxy-TEMPO (TEMPOL), have shown promise in the prevention of cardiovascular dysfunction and programming. This study investigated maternal antioxidant administration with EGCG or TEMPOL and their ability to attenuate the fetal programming of hypertension via Dex injections in WKY rats. Results from this study indicate that, while Dex-programming increased blood pressure in male and female adult offspring, administration of EGCG or TEMPOL via maternal drinking water attenuated Dex-programmed increases in blood pressure, as well as changes in adrenal mRNA and protein levels of catecholamine biosynthetic enzymes phenylalanine hydroxylase (PAH), tyrosine hydroxylase (TH), dopamine beta hydroxylase (DBH), and phenylethanolamine N-methyltransferase (PNMT), in a sex-specific manner. Furthermore, programmed male offspring displayed reduced antioxidant glutathione peroxidase 1 (Gpx1) expression, increased superoxide dismutase 1 (SOD1) and catalase (CAT) expression, and increased pro-oxidant NADPH oxidase activator 1 (Noxa1) expression in the adrenal glands. In addition, prenatal Dex exposure alters expression of epigenetic regulators histone deacetylase (HDAC) 1, 5, 6, 7, 11, in male and HDAC7 in female offspring. These results suggest that glucocorticoids may mediate the fetal programming of hypertension via alteration of epigenetic machinery and oxidative stress pathways.

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Effect of alternate-day fasting therapy combined with Linggui Zhugan Decoction (苓桂术甘汤) on hepatic oxidative stress in hyperlipidemic rat

Chinese Journal of Integrative Medicine ◽

10.1007/s11655-014-1999-8 ◽

2015 ◽

Cited By ~ 2

Author(s):

Jun-jie Zhang ◽

Ying-juan Huang ◽

Bin Ke ◽

Li-ping Liu ◽

Jie-jie Shangguan ◽

...

Keyword(s):

Oxidative Stress ◽

Hepatic Oxidative Stress ◽

Alternate Day Fasting ◽

Linggui Zhugan Decoction

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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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