Protective effect of obestatin on indomethacin-induced acute gastric ulcer in rats: role of VEGF and TNF-α

2018 ◽  
Vol 35 (3) ◽  
pp. 369
Author(s):  
RehamM Ibrahim ◽  
MonaM Allam ◽  
OlaA El-Gohary ◽  
AlaaE.A El-Talees ◽  
MohamedS El-Hamady
Keyword(s):  
Gastric Ulcer ◽  
Protective Effect ◽  
Tnf Α

scholarly journals Role of endogenous TNF-α in cardiomyocyte apoptosis induced by bacteria lipoprotein and the protective effect of IL-10

2015 ◽  
Vol 13 (2) ◽  
pp. 117-125 ◽  
Author(s):  
Zhicai Li ◽  
Jing Zhou ◽  
Dongmei Zhu ◽  
Qian Zhang ◽  
Min Huang ◽  
...  
Keyword(s):  
Protective Effect ◽  
Cardiomyocyte Apoptosis ◽  
Tnf Α

scholarly journals Klotho protects chondrocyte viability via FOXO1/3 in osteoarthritis

2021 ◽  
Vol 20 (9) ◽  
pp. 1961-1968
Author(s):  
Wei Wei ◽  
Liefeng Ji ◽  
Wanli Duan ◽  
Jiang Zhu
Keyword(s):  
Oxidative Stress ◽  
Survival Rate ◽  
Protective Effect ◽  
Collagen I ◽  
Inflammatory Factors ◽  
Ros Production ◽  
Chondrocyte Viability ◽  
Tnf Α ◽  
Collagen Ii

Purpose: To investigate the effect of Klotho and FOXO1/3 on the CH viability in OA.Methods: The survival rate of CHs, Klotho and FOXO1/3 protein expression, and ROS production were measured in the OA cartilages of different degenerative phases. H2O2 was also used to injure CHs, and the cell viability, Klotho and FOXO1/3 expressions, as well as ROS levels were investigated to clarify the effect of exogenic Klotho on the injured CHs. Additionally, in order to verify the role of FOXO1/3 in Klotho-treated CHs, SOD2, GPX1, inflammatory factors, collagen I/II, SOX9, and Runx-2 levels were analyzed by silencing FOXO1 and FOXO3 expression via siRNA transfection.Results: Klotho and FOXO1/3 expressions significantly decreased, and ROS production increased in severely human OA cartilage (p <0.05). Besides, H2O2 affected CHs viability with the suppression of Klotho and FOXO1/3 expression but ROS production was elevated. Exogenic Klotho application partly reversed the injury caused by H2O2. Furthermore, Klotho treatment of the injured CHs contributed to SOD2 and GPX1 expressions, and suppressed IL-1β, IL-6, TNF-α and MMP-13 production, resulting in  the upregulation of collagen II and SOX9 as well as downregulation of collagen I and Runx-2. However, the protective effect of Klotho was weakened by FOXO1 and FOXO3 gene silencing.Conclusion: Klotho protects CHs viability by suppressing oxidative stress and inflammation, which is associated with the mediation of FOXO1 and FOXO3. These findings provide new insights into the treatment of OA.

Activation of cAMP-guanine exchange factor confers PKA-independent protection from hepatocyte apoptosis

2004 ◽  
Vol 287 (2) ◽  
pp. G334-G343 ◽  
Author(s):  
Kimberly A. Cullen ◽  
John McCool ◽  
M. Sawkat Anwer ◽  
Cynthia R. L. Webster
Keyword(s):  
Bile Acid ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Fas Ligand ◽  
Kinase Inhibitor ◽  
Pi3 Kinase ◽  
Akt Phosphorylation ◽  
Tnf Α ◽  
Induced Apoptosis

cAMP has previously been shown to promote cell survival in a variety of cell types, but the downstream signaling pathway(s) of this antiapoptotic effect is unclear. Thus the role of cAMP signaling through PKA and cAMP-regulated guanine nucleotide exchange factors (cAMP-GEFs) in cAMP's antiapoptotic action was investigated in the present study. cAMP's protective effect against bile acid-, Fas ligand-, and TNF-α-induced apoptosis in rat hepatocytes was largely unaffected by the selective PKA inhibitor, Rp-8-(4-chlorophenylthio)-cAMP (Rp-cAMP). In contrast, a novel cAMP analog, 8-(4-chlorophenylthio)-2′- O-methyl (CPT-2-Me)-cAMP, which activated cAMP-GEFs in hepatocytes without activating PKA, protected hepatocytes against apoptosis induced by bile acids, Fas ligand, and TNF-α. The role of cAMP-GEF and PKA on activation of Akt, a kinase implicated in cAMP survival signaling, was investigated. Inhibition of PKA with RP-cAMP had no effect on cAMP-mediated Akt phosphorylation, whereas CPT-2-Me-cAMP, which did not activate PKA, induced phosphatidylinositol 3-kinase (PI3-kinase)-dependent activation of Akt. Pretreatment of hepatocytes with the PI3-kinase inhibitor, Ly-294002, prevented CPT-2-Me-cAMP's protective effect against bile acid and Fas ligand, but not TNF-α-mediated apoptosis. Glucagon, CPT-cAMP, and CPT-2-Me-cAMP all activated Rap 1, a downstream effector of cAMP-GEF. These results suggest that a PKA-independent cAMP/cAMP-GEF/Rap pathway exists in hepatocytes and that activation of cAMP-GEFs promotes Akt phosphorylation and hepatocyte survival. Thus a cAMP/cAMP-GEF/Rap/PI3-kinase/Akt signaling pathway may confer protection against bile acid- and Fas-induced apoptosis in hepatocytes.

Role of cytokines in caerulein-induced acute pancreatilis of IL-1, IL-6 and TNF-α knockoul mice

2001 ◽  
Vol 120 (5) ◽  
pp. A541-A541
Author(s):  
K KITAMURA ◽  
J NIIKAWA ◽  
T IMAMURA ◽  
A TAKAHASHI ◽  
A IKEGAMI ◽  
...  
Keyword(s):  
Tnf Α

Protective effect of the new compound — salicyl-carnosine — on the formation of chronic acetate gastric ulcer in rats*

2019 ◽  
Vol 163 (3) ◽  
pp. 58-64
Author(s):  
I.E. Trubitsyna ◽  
◽  
S.L. Stvolinsky ◽  
O.I. Kulikova ◽  
T.N. Fedorova ◽  
...  
Keyword(s):  
Gastric Ulcer ◽  
Protective Effect

The Role of IL-1, IL-6, TNF-α and MIF in Relative Adrenal Insufficiency in Septic Shock: A Study in Piglet Model

2018 ◽  
Author(s):  
Bina Akura ◽  
Jose Batubara ◽  
Zakiudin Munasir ◽  
Gunati unknown ◽  
Joedo Prihartono ◽  
...  
Keyword(s):  
Septic Shock ◽  
Adrenal Insufficiency ◽  
Relative Adrenal Insufficiency ◽  
Tnf Α

Inhibition of microRNA-155 Alleviates Neurological Dysfunction Following Transient Global Ischemia and Contribution of Neuroinflammation and Oxidative Stress in the Hippocampus

2020 ◽  
Vol 25 (40) ◽  
pp. 4310-4317 ◽  
Author(s):  
Lichao Sun ◽  
Shouqin Ji ◽  
Jihong Xing
Keyword(s):  
Oxidative Stress ◽  
Brain Edema ◽  
Severity Score ◽  
Global Ischemia ◽  
Signal Pathways ◽  
Neurological Severity Score ◽  
Tnf Α ◽  
Transient Global Ischemia ◽  
And Oxidative Stress

Background/Aims: Central pro-inflammatory cytokine (PIC) signal is involved in neurological deficits after transient global ischemia induced by cardiac arrest (CA). The present study was to examine the role of microRNA- 155 (miR-155) in regulating IL-1β, IL-6 and TNF-α in the hippocampus of rats with induction of CA. We further examined the levels of products of oxidative stress 8-isoprostaglandin F2α (8-iso PGF2α, indication of oxidative stress); and 8-hydroxy-2’-deoxyguanosine (8-OHdG, indication of protein oxidation) after cerebral inhibition of miR-155. Methods: CA was induced by asphyxia and followed by cardiopulmonary resuscitation in rats. ELISA and western blot analysis were used to determine the levels of PICs and products of oxidative stress; and the protein expression of NADPH oxidase (NOXs) in the hippocampus. In addition, neurological severity score and brain edema were examined to assess neurological functions. Results: We observed amplification of IL-1β, IL-6 and TNF-α along with 8-iso PGF2α and 8-OHdG in the hippocampus of CA rats. Cerebral administration of miR-155 inhibitor diminished upregulation of PICs in the hippocampus. This also attenuated products of oxidative stress and upregulation of NOX4. Notably, inhibition of miR-155 improved neurological severity score and brain edema and this was linked to signal pathways of PIC and oxidative stress. Conclusion: We showed the significant role of blocking miR-155 signal in improving the neurological function in CA rats likely via inhibition of signal pathways of neuroinflammation and oxidative stress, suggesting that miR-155 may be a target in preventing and/or alleviating development of the impaired neurological functions during CA-evoked global cerebral ischemia.

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