THAP11 down-regulation may contribute to cardio-protective effects of sevoflurane anesthesia: Evidence from clinical and molecular evidence

Life Sciences ◽  
2021 ◽  
Vol 274 ◽  
pp. 119327
Author(s):  
Zhenxin Duan ◽  
Xiaoying Zhou ◽  
Feng Chen ◽  
Huifang Chen ◽  
Guangyou Duan ◽  
...  
Keyword(s):  
Molecular Evidence ◽  
Protective Effects ◽  
Sevoflurane Anesthesia ◽  
Down Regulation

scholarly journals NAFLD, Estrogens, and Physical Exercise: The Animal Model

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Jean-Marc Lavoie ◽  
Abdolnaser Pighon
Keyword(s):  
Animal Model ◽  
Exercise Training ◽  
Postmenopausal Women ◽  
Liver Fat ◽  
Molecular Evidence ◽  
Protective Effects ◽  
Fat Accumulation ◽  
Present Information ◽  
Nonalcoholic Hepatic Steatosis

One segment of the population that is particularly inclined to liver fat accumulation is postmenopausal women. Although nonalcoholic hepatic steatosis is more common in men than in women, after menopause there is a reversal in gender distribution. At the present time, weight loss and exercise are regarded as first line treatments for NAFLD in postmenopausal women, as it is the case for the management of metabolic syndrome. In recent years, there has been substantial evidence coming mostly from the use of the animal model, that indeed estrogens withdrawal is associated with modifications of molecular markers favouring the activity of metabolic pathways ultimately leading to liver fat accumulation. In addition, the use of the animal model has provided physiological and molecular evidence that exercise training provides estrogens-like protective effects on liver fat accumulation and its consequences. The purpose of the present paper is to present information relative to the development of a state of NAFLD resulting from the absence of estrogens and the role of exercise training, emphasizing on the contribution of the animal model on these issues.

scholarly journals Novel Molecular Evidence Related to COVID-19 in Patients with Diabetes Mellitus

2020 ◽  
Vol 9 (12) ◽  
pp. 3962
Author(s):  
Yu-Huang Liao ◽  
Jing-Quan Zheng ◽  
Cai-Mei Zheng ◽  
Kuo-Cheng Lu ◽  
You-Chen Chao
Keyword(s):  
Diabetes Mellitus ◽  
Viral Entry ◽  
Cell Injury ◽  
Molecular Evidence ◽  
Protective Effects ◽  
Cytosolic Ph ◽  
S Protein ◽  
Patients With Diabetes ◽  
Type 1 Dm

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has rapidly evolved into a global pandemic. The hyperglycemia in patients with diabetes mellitus (DM) substantially compromises their innate immune system. SARS-CoV-2 uses human angiotensin-converting enzyme 2 (ACE2) receptors to enter the affected cell. Uncontrolled hyperglycemia-induced glycosylation of ACE2 and the S protein of SARS-CoV-2 could facilitate the binding of S protein to ACE2, enabling viral entry. Downregulation of ACE2 activity secondary to SARS-CoV-2 infection, with consequent accumulation of angiotensin II and metabolites, eventually leads to poor outcomes. The altered binding of ACE2 with SARS-CoV-2 and the compromised innate immunity of patients with DM increase their susceptibility to COVID-19; COVID-19 induces pancreatic β-cell injury and poor glycemic control, which further compromises the immune response and aggravates hyperglycemia and COVID-19 progression, forming a vicious cycle. Sequential cleavage of viral S protein by furin and transmembrane serine protease 2 (TMPRSS2) triggers viral entry to release the viral genome into the target cell. Hence, TMPRSS2 and furin are possible drug targets. As type 1 DM exhibits a Th1-driven autoimmune process, the relatively lower mortality of COVID-19 in type 1 DM compared to type 2 DM might be attributed to an imbalance between Th1 and Th2 immunity. The anti-inflammatory effects of dipeptidyl peptidase-4 inhibitor may benefit patients with DM and COVID-19. The potential protective effects of sodium–glucose cotransporter-2 inhibitor (SGLT2i), including reduction in lactate level, prevention of lowering of cytosolic pH and reduction in pro-inflammatory cytokine levels may justify the provision of SGLT2i to patients with DM and mild or asymptomatic COVID-19. For patients with DM and COVID-19 who require hospitalization, insulin-based treatment is recommended with cessation of metformin and SGLT2i. Further evidence from randomized or case–control clinical trials is necessary to elucidate the effectiveness and pitfalls of different types of medication for DM.

scholarly journals Cellular and Molecular Evidence of Acetaldehyde Elimination and Intracellular Environment Antioxidation by L-Cysteine

2018 ◽  
Vol 2018 ◽  
pp. 1-8
Author(s):  
Zhenjing Li ◽  
Xiaohong Zhang ◽  
Yibin Xue ◽  
Jingkai Zhang ◽  
Meiling Li ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
A549 Cells ◽  
Control Group ◽  
Molecular Evidence ◽  
Protective Mechanism ◽  
Colorimetric Determination ◽  
Dependent Manner ◽  
Protective Effects ◽  
Dapi Staining ◽  
Dose Dependent

Acetaldehyde is a harmful metabolite of smoking and drinking. This study was initially intended to facilitate the understanding of the possible injury mechanism of A549 cells damaged by acetaldehyde and the possible protective mechanism of L-cysteine (L-Cys) by analyzing the oxidative damage indicators, as well as the changes in cell morphology and gene expression. Results from the dithiodimorpholine nitrobenzoic acid colorimetric determination for glutathione peroxidase (GSH-Px) activity in L-Cys groups were significantly higher (P<0.01) than those in the acetaldehyde group in a dose-dependent manner. The expression of cytochrome c oxidase subunit II (COII) mRNA was significantly reduced compared with the control group (P<0.01) and was noticeably restored in the L-Cys groups. Scanning electronic microscopy observation, DAPI staining, and flow cytometry also indicated that L-Cys could effectively attenuate the oxidative damage to A549 cells caused by acetaldehyde and reduces the rate of apoptosis. In conclusion, the protective effects of L-Cys on A549 cells against oxidative damage by acetaldehyde were dose-dependent within the range of 10 μmol/L to 160 μmol/L. Acetaldehyde damaged the mitochondria and resulted in the apoptosis of A549 cells by reactive oxygen species (ROS), e.g., free radicals, but L-Cys reversed the release of cytochrome c from the mitochondria, reduced the rate of apoptosis, and protected cells from ROS and oxidative stress.

scholarly journals Protective effects of seaweed supplemented diet on antioxidant and immune responses in European seabass (Dicentrarchus labrax) subjected to bacterial infection

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Maria J. Peixoto ◽  
Renato Ferraz ◽  
Leonardo J. Magnoni ◽  
Rui Pereira ◽  
José F. Gonçalves ◽  
...  
Keyword(s):  
Bacterial Infection ◽  
Antioxidant Capacity ◽  
Bacterial Infections ◽  
Control Diet ◽  
Dicentrarchus Labrax ◽  
Head Kidney ◽  
Protective Effects ◽  
Down Regulation ◽  
Antioxidant Genes ◽  
European Seabass

Abstract European seabass (Dicentrarchus labrax) production is often hampered by bacterial infections such as photobacteriosis caused by Photobacterium damselae subsp. piscicida (Phdp). Since diet can impact fish immunity, this work investigated the effect of dietary supplementation of 5% Gracilaria sp. aqueous extract (GRA) on seabass antioxidant capacity and resistance against Phdp. After infection, mortality was delayed in fish fed GRA, which also revealed increased lysozyme activity levels, as well as decreased lipid peroxidation, suggesting higher antioxidant capacity than in fish fed a control diet. Dietary GRA induced a down-regulation of hepatic stress-responsive heat shock proteins (grp-78, grp-170, grp-94, grp-75), while bacterial infection caused a down-regulation in antioxidant genes (prdx4 and mn-sod). Diet and infection interaction down-regulated the transcription levels of genes associated with oxidative stress response (prdx5 and gpx4) in liver. In head-kidney, GRA led to an up-regulation of genes associated with inflammation (il34, ccr9, cd33) and a down-regulation of genes related to cytokine signalling (mif, il1b, defb, a2m, myd88). Additionally, bacterial infection up-regulated immunoglobulins production (IgMs) and down-regulated the transcription of the antimicrobial peptide leap2 in head kidney. Overall, we found that GRA supplementation modulated seabass resistance to Phdp infection.

scholarly journals Platycodin D enhances LDLR expression and LDL uptake via down-regulation of IDOL mRNA in hepatic cells

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yu-Jeong Choi ◽  
Sol Ji Lee ◽  
Hyo In Kim ◽  
Hee Jung Lee ◽  
So Jung Kang ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Synergistic Effects ◽  
Biological Activities ◽  
Therapeutic Option ◽  
Molecular Evidence ◽  
Triterpenoid Saponin ◽  
Atherosclerotic Cardiovascular Disease ◽  
Down Regulation ◽  
Hepatic Cells

AbstractThe root of Platycodon grandiflorum (PG) has long been used as a traditional herbal medicine in Asian country. Platycondin D (PD), triterpenoid saponin that is a main constituent of PG, exhibits various biological activities such as anti-inflammatory, anti-oxidant, anti-diabetic, and anti-cancer effects. A previous study showed that PD had cholesterol-lowering effects in mice that develop hypercholesterolemia, but the underlying molecular mechanisms have not been elucidated during the last decade. Here, we demonstrated that both PG and PD markedly increased levels of cell surface low-density lipoprotein receptor (LDLR) by down-regulation of the E3 ubiquitin ligase named inducible degrader of the LDLR (IDOL) mRNA, leading to the enhanced uptake of LDL-derived cholesterol (LDL-C) in hepatic cells. Furthermore, cycloheximide chase analysis and in vivo ubiquitination assay revealed that PD increased the half-life of LDLR protein by reducing IDOL-mediated LDLR ubiquitination. Finally, we demonstrated that treatment of HepG2 cells with simvastatin in combination with PG and PD had synergistic effects on the improvement of LDLR expression and LDL-C uptake. Together, these results provide the first molecular evidence for anti-hypercholesterolemic activity of PD and suggest that PD alone or together with statin could be a potential therapeutic option in the treatment of atherosclerotic cardiovascular disease.

Protective effects of PARP inhibitor, PJ34, is related to down-regulation of calpain and NF-κB in a mouse model of TBI

Brain Injury ◽  
2016 ◽  
pp. 1-11 ◽  
Author(s):  
Xiaogang Tao ◽  
Xuetao Chen ◽  
Xiang Mao ◽  
Zonggang Hou ◽  
Shuyu Hao ◽  
...  
Keyword(s):  
Mouse Model ◽  
Parp Inhibitor ◽  
Protective Effects ◽  
Down Regulation
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