scholarly journals Potential COVID-19 Immunomodulators and Beyond: NSAIDs Might Inhibit SARS CoV-2 ORF Proteins Induced Caspase Activation, Necroptosis and Endoplasmic Reticulum Stress.

2021 ◽  
Author(s):  
Mina Kelleni
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Caspase Activation ◽  
First Choice ◽  
Anti Inflammatory ◽  
One Year

We have previously suggested numerous immunomodulatory and anti-inflammatory benefits when NSAIDs are administered as first choice therapy early in management of COVID-19 and in this manuscript we add several additional clues and it is really unfortunate that for more than one year of relentless struggle, this call is not yet adopted to save precious lives that are succumbed every day.

scholarly journals NSAIDs Immunomodulation in COVID-19 Might Inhibit SARS CoV-2 ORF Proteins Induced Caspase Activation, Necroptosis and Endoplasmic Reticulum Stress.

2021 ◽  
Author(s):  
Mina Kelleni
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Mitochondrial Dysfunction ◽  
Caspase Activation ◽  
Caspase Inhibitors ◽  
Caspase Recruitment Domain ◽  
Signaling Mechanisms ◽  
First Choice ◽  
Potential Benefits ◽  
One Year

We have previously suggested numerous immunomodulatory and anti-inflammatory benefits when NSAIDs are administered to manage COVID-19 and in this commentary, we add other potential benefits related to SARS CoV-2 ORF proteins dependent activation of caspases with subsequent mitochondrial dysfunction, endoplasmic reticulum stress and necroptosis that were described with complicated COVID-19 as NSAIDs are known to be caspase inhibitors. Moreover, NSAIDs might independently inhibit other COVID-19 associated downstream pathological signaling mechanisms. We also postulate that CARD-14, a caspase recruitment domain-containing protein, polymorphisms might play a role in development of severe and critical COVID-19. We believe that it is very unfortunate that for more than one year of relentless struggle, our recommendation to adopt NSAIDs as first choice COVID-19 therapy has not adopted while lives are lost are succumbed every day.

scholarly journals NSAIDs Immunomodulation in COVID-19 Might Inhibit SARS CoV-2 ORF Proteins Induced Caspase Activation, Necroptosis and Endoplasmic Reticulum Stress.

2021 ◽  
Author(s):  
Mina Kelleni
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Mitochondrial Dysfunction ◽  
Caspase Activation ◽  
Caspase Inhibitors ◽  
Caspase Recruitment Domain ◽  
Signaling Mechanisms ◽  
First Choice ◽  
Potential Benefits ◽  
One Year

We have previously suggested numerous immunomodulatory and anti-inflammatory benefits when NSAIDs are administered to manage COVID-19 and in this commentary, we add other potential benefits related to SARS CoV-2 ORF proteins dependent activation of caspases with subsequent mitochondrial dysfunction, endoplasmic reticulum stress and necroptosis that were described with complicated COVID-19 as NSAIDs are known to be caspase inhibitors. Moreover, NSAIDs might independently inhibit other COVID-19 associated downstream pathological signaling mechanisms. We also postulate that CARD-14, a caspase recruitment domain-containing protein, polymorphisms might play a role in development of severe and critical COVID-19. We believe that it is very unfortunate that for more than one year of relentless struggle, our recommendation to adopt NSAIDs as first choice COVID-19 therapy has not adopted while lives are lost are succumbed every day.

scholarly journals NSAIDs Immunomodulation in COVID-19 Might Inhibit SARS CoV-2 ORF Proteins Induced Caspase Activation, Necroptosis and Endoplasmic Reticulum Stress.

2021 ◽  
Author(s):  
Mina Kelleni
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Mitochondrial Dysfunction ◽  
Caspase Activation ◽  
Caspase Inhibitors ◽  
Caspase Recruitment Domain ◽  
Signaling Mechanisms ◽  
First Choice ◽  
Potential Benefits ◽  
One Year

We have previously suggested numerous immunomodulatory and anti-inflammatory benefits when NSAIDs are administered to manage COVID-19 and in this commentary, we add other potential benefits related to SARS CoV-2 ORF proteins dependent activation of caspases with subsequent mitochondrial dysfunction, endoplasmic reticulum stress and necroptosis that were described with complicated COVID-19 as NSAIDs are known to be caspase inhibitors. Moreover, NSAIDs might independently inhibit other COVID-19 associated downstream pathological signaling mechanisms. We also postulate that CARD-14, a caspase recruitment domain-containing protein, polymorphisms might play a role in development of severe and critical COVID-19. We believe that it is very unfortunate that for more than one year of relentless struggle, our recommendation to adopt NSAIDs as first choice COVID-19 therapy has not adopted while lives are lost are succumbed every day.

scholarly journals Methane Alleviates Acetaminophen-Induced Liver Injury by Inhibiting Inflammation, Oxidative Stress, Endoplasmic Reticulum Stress, and Apoptosis through the Nrf2/HO-1/NQO1 Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Yang Feng ◽  
Ruixia Cui ◽  
Zeyu Li ◽  
Xia Zhang ◽  
Yifan Jia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Liver Injury ◽  
Endoplasmic Reticulum Stress ◽  
Signaling Pathway ◽  
Hepatic Injury ◽  
Protective Effects ◽  
Serum Aminotransferase ◽  
Anti Inflammatory

Acetaminophen- (APAP-) induced hepatic injury is an important clinical challenge. Oxidative stress, inflammation, apoptosis, and endoplasmic reticulum stress (ERS) contribute to the pathogenesis. Methane has potential anti-inflammatory, antioxidant, and antiapoptotic properties. This project was aimed at studying the protective effects and relative mechanisms of methane in APAP-induced liver injury. In the in vivo experiment, C57BL/6 mice were treated with APAP (400 mg/kg) to induce hepatic injury followed by methane-rich saline (MRS) 10 ml/kg i.p. after 12 and 24 h. We observed that MRS alleviated the histopathological lesions in the liver, decreased serum aminotransferase levels, reduced the levels of inflammatory cytokines, suppressed the nuclear factor-κB expression. Further, we found that MRS relieved oxidative stress by regulating the Nrf2/HO-1/NQO1 signaling pathway and their downstream products after APAP challenge. MRS also regulated proteins associated with ERS-induced apoptosis. In the in vitro experiment, the L-02 cell line was treated with APAP (10 mM) to induce hepatic injury. We found that a methane-rich medium decreased the levels of reactive oxygen species (DHE fluorescent staining), inhibited apoptosis (cell flow test), and regulated the Nrf2/HO-1/NQO1 signaling pathway. Our data indicated that MRS prevented APAP-induced hepatic injury via anti-inflammatory, antioxidant, anti-ERS, and antiapoptotic properties involving the Nrf2/HO-1/NQO1 signaling pathway.

Endoplasmic reticulum stress induced apoptosis and caspase activation is mediated through mitochondria during megakaryocyte differentiation

Mitochondrion ◽  
2020 ◽  
Vol 50 ◽  
pp. 115-120 ◽  
Author(s):  
Narasaiah Kovuru ◽  
Sanjeev Raghuwanshi ◽  
Durga Shankar Sharma ◽  
Swati Dahariya ◽  
Adithya Pallepati ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Caspase Activation ◽  
Induced Apoptosis ◽  
Megakaryocyte Differentiation

scholarly journals Isoflurane induces endoplasmic reticulum stress and caspase activation through ryanodine receptors

2014 ◽  
Vol 113 (4) ◽  
pp. 695-707 ◽  
Author(s):  
H. Wang ◽  
Y. Dong ◽  
J. Zhang ◽  
Z. Xu ◽  
G. Wang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Ryanodine Receptors ◽  
Caspase Activation

scholarly journals Melatonin Induces Anti-Inflammatory Effects to Play a Protective Role via Endoplasmic Reticulum Stress in Acute Pancreatitis

2016 ◽  
Vol 40 (5) ◽  
pp. 1094-1104 ◽  
Author(s):  
Yina Chen ◽  
Jie Zhang ◽  
Qian Zhao ◽  
Qinfen Chen ◽  
Yangjie Sun ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Western Blotting ◽  
Early Stage ◽  
Protective Role ◽  
Rat Models ◽  
Ar42j Cell ◽  
Anti Inflammatory ◽  
The Relationship

Background/Aims: Melatonin, which is mainly secreted by the pineal gland and released into blood, has anti-inflammatory properties in acute pancreatitis. Many studies show that melatonin can relieve inflammation in taurocholate-induced acute pancreatitis. However, the mechanisms of its anti-inflammatory effects are still undefined, especially the relationship between melatonin and endoplasmic reticulum stress. We explored the anti-inflammatory activity of melatonin in AR42J and rat models. Methods: The CCK-8 assay was used to assess effects of melatonin on AR42J cell viability. Inflammatory degree and the expressions of endoplasmic reticulum stress related molecules were examined by quantitative RT-PCR and western blotting. The degree of inflammation in the tissue was also accessed by pathological grading. Finally, we used the western blotting method to verify apoptosis and autophagy. Results: Endoplasmic reticulum stress was obviously activated in early stage inflammation in AR42J and rat models. Melatonin could induce anti-inflammatory effects via endoplasmic reticulum stress. Melatonin significantly inhibited inflammatory cytokines and the expression of ERS-related molecules. Finally, it played a protective role by promoting apoptosis and autophagy of the cells, which were damaged in the process of inflammatory reaction. Conclusion: Melatonin induces anti-inflammatory effects via endoplasmic reticulum stress in acute pancreatitis to play a protective role.

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