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

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

scholarly journals Vitamin D Deficiency Aggravates Hepatic Oxidative Stress and Inflammation during Chronic Alcohol-Induced Liver Injury in Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Chun-Qiu Hu ◽  
Qing-Li Bo ◽  
Lan-Lan Chu ◽  
Yong-Di Hu ◽  
Lin Fu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Liver Injury ◽  
Vitamin D Deficiency ◽  
Chronic Alcohol ◽  
Cytokines And Chemokines ◽  
Hepatic Oxidative Stress ◽  
Oxide Synthase ◽  
Etoh Group ◽  
Inducible Nitric Oxide

Vitamin D deficiency has been reported in alcoholics. This study is aimed at evaluating the effects of vitamin D deficiency on chronic alcohol-induced liver injury in mice. Mice were fed with modified Lieber-DeCarli liquid diets for 6 weeks to establish an animal model of chronic alcohol-induced liver injury. In the VDD+EtOH group, mice were fed with modified diets, in which vitamin D was depleted. Vitamin D deficiency aggravated alcohol-induced liver injury. Furthermore, vitamin D deficiency aggravated hepatocyte apoptosis during alcohol-induced liver injury. Although it has a little effect on hepatic TG content, vitamin D deficiency promoted alcohol-induced hepatic GSH depletion and lipid peroxidation. Further analysis showed that vitamin D deficiency further increased alcohol-induced upregulation of hepatic inducible nitric oxide synthase (inos), two NADPH oxidase subunits p47phox and gp91phox, and heme oxygenase- (HO-) 1. By contrast, vitamin D deficiency attenuated alcohol-induced upregulation of hepatic antioxidant enzyme genes, such as superoxide dismutase (sod) 1 and gshpx. In addition, vitamin D deficiency significantly elevated alcohol-induced upregulation of hepatic proinflammatory cytokines and chemokines. Taken together, these results suggest that vitamin D deficiency aggravates hepatic oxidative stress and inflammation during chronic alcohol-induced liver injury.

Polysaccharides from Enteromorpha prolifera protect against carbon tetrachloride-induced acute liver injury in mice via activation of Nrf2/HO-1 signaling, and suppression of oxidative stress, inflammation and apoptosis

2020 ◽  
Vol 11 (5) ◽  
pp. 4485-4498
Author(s):  
Fuchuan Guo ◽  
Xinyun Zhuang ◽  
Mengyuan Han ◽  
Wenting Lin
Keyword(s):  
Oxidative Stress ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Hepatic Injury ◽  
Acute Liver Injury ◽  
Reactive Intermediates ◽  
Enteromorpha Prolifera ◽  
Hepatic Oxidative Stress

EPP protected against hepatic injury induced by CCl4-derived reactive intermediates through the suppression of hepatic oxidative stress, inflammation, and apoptosis.

Sinomenine attenuates alcohol-induced acute liver injury via inhibiting oxidative stress, inflammation and apoptosis in mice

2021 ◽  
pp. 112759
Author(s):  
Hui Fan ◽  
Tingting Tu ◽  
Xiao Zhang ◽  
Qiankun Yang ◽  
Jinxin Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Acute Liver Injury

Role of Vitamins in Neurodegenerative Diseases: A Review

2021 ◽  
Vol 20 ◽  
Author(s):  
Ravi Ranjan Kumar ◽  
Lovekesh Singh ◽  
Amandeep Thakur ◽  
Shamsher Singh ◽  
Bhupinder Kumar
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Vitamin D ◽  
Vitamin C ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Vitamin D Deficiency ◽  
Neurological Disorders ◽  
The Brain

Background: Vitamins are the micronutrients required for boosting the immune system and managing any future infection. Vitamins are involved in neurogenesis, a defense mechanism working in neurons, metabolic reactions, neuronal survival, and neuronal transmission. Their deficiency leads to abnormal functions in the brain like oxidative stress, mitochondrial dysfunction, accumulation of proteins (synuclein, Aβ plaques), neurodegeneration, and excitotoxicity. Methods: In this review, we have compiled various reports collected from PubMed, Scholar Google, Research gate, and Science direct. The findings were evaluated, compiled, and represented in this manuscript. Conclusion: The deficiency of vitamins in the body causes various neurological disorders like Alzheimer’s disease, Parkinson’s disease, Huntington's disease, and depression. We have discussed the role of vitamins in neurological disorders and the normal human body. Depression is linked to a deficiency of vitamin-C and vitamin B. In the case of Alzheimer’s disease, there is a lack of vitamin-B1, B12, and vitamin-A, which results in Aβ-plaques. Similarly, in Parkinson’s disease, vitamin-D deficiency leads to a decrease in the level of dopamine, and imbalance in vitamin D leads to accumulation of synuclein. In MS, Vitamin-C and Vitamin-D deficiency causes demyelination of neurons. In Huntington's disease, vitamin- C deficiency decreases the antioxidant level, enhances oxidative stress, and disrupts the glucose cycle. Vitamin B5 deficiency in Huntington's disease disrupts the synthesis of acetylcholine and hormones in the brain.

scholarly journals The Late-Stage Protective Effect of Mito-TEMPO against Acetaminophen-Induced Hepatotoxicity in Mouse and Three-Dimensional Cell Culture Models

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 965
Author(s):  
Mohammad Abdullah-Al-Shoeb ◽  
Kenta Sasaki ◽  
Saori Kikutani ◽  
Nanami Namba ◽  
Keiichi Ueno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Culture ◽  
Liver Injury ◽  
Protective Effect ◽  
Acute Liver Injury ◽  
Three Dimensional ◽  
3D Cell Culture ◽  
Cell Culture Model ◽  
Culture Model ◽  
Apap Hepatotoxicity

An overdose of acetaminophen (APAP), the most common cause of acute liver injury, induces oxidative stress that subsequently causes mitochondrial impairment and hepatic necroptosis. N-acetyl-L-cysteine (NAC), the only recognized drug against APAP hepatotoxicity, is less effective the later it is administered. This study evaluated the protective effect of mitochondria-specific Mito-TEMPO (Mito-T) on APAP-induced acute liver injury in C57BL/6J male mice, and a three dimensional (3D)-cell culture model containing the human hepatoblastoma cell line HepG2. The administration of Mito-T (20 mg/kg, i.p.) 1 h after APAP (400 mg/kg, i.p.) injection markedly attenuated the APAP-induced elevated serum transaminase activity and hepatic necrosis. However, Mito-T treatment did not affect key factors in the development of APAP liver injury including the activation of c-jun N-terminal kinases (JNK), and expression of the transcription factor C/EBP homologous protein (CHOP) in the liver. However, Mito-T significantly reduced the APAP-induced increase in the hepatic oxidative stress marker, nitrotyrosine, and DNA fragmentation. Mito-T markedly attenuated cytotoxicity induced by APAP in the HepG2 3D-cell culture model. Moreover, liver regeneration after APAP hepatotoxicity was not affected by Mito-T, demonstrated by no changes in proliferating cell nuclear antigen formation. Therefore, Mito-T was hepatoprotective at the late-stage of APAP overdose in mice.

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