scholarly journals Esomeprazole alleviates the damage to stress ulcer in rats through not only its antisecretory effect but its antioxidant effect by inactivating the p38 MAPK and NF-κB signaling pathways

2019 ◽  
Vol Volume 13 ◽  
pp. 2969-2984 ◽  
Author(s):  
Wei Xie ◽  
Xielin Huang ◽  
Renpin Chen ◽  
Ruru Chen ◽  
Tang Li ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
P38 Mapk ◽  
Stress Ulcer ◽  
Antioxidant Effect ◽  
Antisecretory Effect

The Impact of Royal Jelly against Hepatic Ischemia/Reperfusion-Induced Hepatocyte Damage in Rats: The Role of Cytoglobin, Nrf-2/HO-1/COX-4, and P38-MAPK/NF-κB-p65/TNF-α Signaling Pathways

2020 ◽  
Vol 14 (1) ◽  
pp. 88-100
Author(s):  
Fares E.M. Ali ◽  
Heba M. Saad Eldien ◽  
Nashwa A.M. Mostafa ◽  
Abdulrahman H. Almaeen ◽  
Mohamed R.A. Marzouk ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
P38 Mapk ◽  
Royal Jelly ◽  
Ischemia Reperfusion ◽  
Histopathological Changes ◽  
Down Regulation ◽  
Hepatic Ischemia ◽  
Tnf Α ◽  
Hepatic Ischemia Reperfusion ◽  
The Impact

Objective: The present study was conducted to elucidate the underlying molecular mechanism as well as the potential hepatoprotective effects of royal jelly (RJ) against hepatic ischemia/reperfusion (IR) injury. Methods: Rats were assigned into four groups; sham (received vehicle), IR (30 minutes ischemia and 45 minutes reperfusion), sham pretreated with RJ (200 mg/kg P.O.), and IR pretreated with RJ (200 mg/kg P.O.). The experiment has lasted for 28 days. Results: Hepatic IR significantly induced hepatic dysfunctions, as manifested by elevation of serum transaminases, ALP and LDH levels. Moreover, hepatic IR caused a significant up-regulation of P38-MAPK, NF-κB-p65, TNF-α and MDA levels along with marked down-regulation of Nrf-2, HO-1, COX-4, cytoglobin, IκBa, IL-10, GSH, GST and SOD levels. Additionally, marked histopathological changes were observed after hepatic IR injury. On the contrary, pretreatment with RJ significantly improved hepatic functions along with the alleviation of histopathological changes. Moreover, RJ restored oxidant/antioxidant balance as well as hepatic expressions of Nrf-2, HO-1, COX-4, and cytoglobin. Simultaneously, RJ significantly mitigated the inflammatory response by down-regulation of P38-MAPK, NF-κB-p65, TNF-α expression. Conclusion: The present results revealed that RJ has successfully protected the liver against hepatic IR injury through modulation of cytoglobin, Nrf-2/HO-1/COX-4, and P38-MAPK/NF-κB-p65/TNF-α signaling pathways.

Trans-ferulic acid ameliorates cisplatin-induced testicular damage via suppression of TLR4, P38-MAPK, and ERK1/2 signaling pathways

2021 ◽  
Author(s):  
Emad H. M. Hassanein ◽  
Basel A. Abdel-Wahab ◽  
Fares E. M. Ali ◽  
Omnia A. M. Abd El-Ghafar ◽  
Magy R. Kozman ◽  
...  
Keyword(s):  
Ferulic Acid ◽  
Signaling Pathways ◽  
P38 Mapk ◽  
Testicular Damage

scholarly journals Lipopolysaccharide activates innate immune responses in murine intestinal myofibroblasts through multiple signaling pathways

2009 ◽  
Vol 296 (3) ◽  
pp. G601-G611 ◽  
Author(s):  
Kristen L. W. Walton ◽  
Lisa Holt ◽  
R. Balfour Sartor
Keyword(s):  
Immune Responses ◽  
Signaling Pathways ◽  
P38 Mapk ◽  
Western Blotting ◽  
Pi3 Kinase ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Fold Induction ◽  
Cox 2 ◽  
Multiple Signaling

Myofibroblasts (MF) play an important role in intestinal wound healing. A compromised epithelial barrier exposes intestinal subepithelial MF to luminal bacterial products. However, responses of murine intestinal MF to bacterial adjuvants and potential roles of intestinal MF in innate immune responses are not well defined. Our aims in this study were to determine innate immune responses and intracellular signaling pathways of intestinal MF exposed to LPS, a prototypic Toll-like receptor (TLR) ligand. Expression of TLR4 in primary murine intestinal MF cultures was confirmed by RT-PCR and Western blotting. LPS-induced secretion of prostaglandin E2 (PGE2), interleukin (IL)-6, and keratinocyte-derived chemokines (KC) was measured by ELISA. Intracellular responses to LPS were assessed by Western blotting for NF-κB p65, Iκ-Bα, Akt, p38 MAP kinase, and cyclooxygenase-2 (COX-2). LPS induced rapid phosphorylation of NF-κB p65, Akt, and p38 MAPK and degradation of Iκ-Bα. LPS induced expression of COX-2 and secretion of PGE2 (2.0 ± 0.8-fold induction vs. unstimulated cells), IL-6 (6.6 ± 0.4-fold induction), and KC (12.5 ± 0.4-fold induction). Inhibition of phosphoinositide-3 (PI3)-kinase, p38 MAPK, or NF-κB pathways reduced LPS-induced PGE2, IL-6, and KC secretion. These studies show that primary murine intestinal MF respond to LPS, evidenced by activation of NF-κB, PI3-kinase, and MAPK signaling pathways and secretion of proinflammatory molecules. Inhibition of these pathways attenuated LPS-dependent PGE2, IL-6, and KC production, indicating that LPS activates MF by multiple signaling pathways. These data support the hypothesis that MF are a component of the innate immune system and may exert paracrine effects on adjacent epithelial and immune cells by responding to luminal bacterial adjuvants.

scholarly journals TGF-β1 targets Smad, p38 MAPK, and PI3K/Akt signaling pathways to induce PFKFB3 gene expression and glycolysis in glioblastoma cells

FEBS Journal ◽  
2017 ◽  
Vol 284 (20) ◽  
pp. 3437-3454 ◽  
Author(s):  
Ana Rodríguez-García ◽  
Paula Samsó ◽  
Pere Fontova ◽  
Helga Simon-Molas ◽  
Anna Manzano ◽  
...  
Keyword(s):  
Gene Expression ◽  
Signaling Pathways ◽  
P38 Mapk ◽  
Akt Signaling ◽  
Glioblastoma Cells ◽  
Tgf Β1
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