Administration of SB239063, a potent p38 MAPK inhibitor, alleviates acute lung injury induced by intestinal ischemia reperfusion in rats associated with AQP4 downregulation

Xiong, Liu‐Lin; Tan, Yan; Ma, Hongyu; Dai, Pengcheng; Qin, Yanxia; Yang, Rui-ai; Xu, Yanyan; Deng, Zheng; Zhao, Wei; Xia, Qinjie; Wang, Ting‐Hua; Zhang, Yunhui

doi:10.1016/j.intimp.2016.03.036

Cited by 41 publications

(26 citation statements)

References 47 publications

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“…In our study, we found out that the protein level of p‐p38MAPK was significantly higher in the blood sample of patients with MODS and the p‐p38MAPK induced by serum from patients with MODS was also significantly increased compared to control group ( P < 0.05). Study demonstrated that cellular toxins and pro‐inflammatory factors, such as IL‐1 and TNF‐α, could activate the signaling pathway of p38MAPK, while blocking the p38MAPK signaling pathway could alleviate the inflammatory response, restraining the production of IL‐1 and TNF‐α . These results together indicated that activation of the p38MAPK signaling pathway was involved in the process of intestinal barrier dysfunction in patients with MODS, and p38MAPK activation may be associated with the release of the inflammatory factors in patients with MODS.…”

Section: Discussionmentioning

confidence: 85%

The effect of continuous blood purification on P38MAPK signaling pathway in patients with multiple organ dysfunction syndrome

Pan

2019

Clinical Laboratory Analysis

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Objective The aim of the study was to investigate the role of p38MAPK signaling pathway in patients with multiple organ dysfunction syndrome treated with continuous blood purification. Methods Blood samples were obtained to analyze the protein level of inflammatory factors (IL‐1, IL‐8, IL‐10, and TNF‐α) and phosphorylated p38MAPK by utilizing ELISA assay and Western blotting, respectively. The relative mRNA level of iNOS was detected by using RT‐PCR. In vitro study was conducted in Caco‐2 cells, which were treated with serum from patients subjected to continuous blood purification. Serum‐induced inflammatory factors and phosphorylated p38MAPK were also analyzed in Caco‐2 cells. Results The protein levels of IL‐1, IL‐8, IL‐10, and TNF‐α were significantly decreased in Caco‐2 cells treated with serum obtained from patients who were subjected to continuous blood purification therapy at the time course of 12 and 24 hours. A drastic decrease (P < 0.05) was observed in the level of IL‐8 and TNF‐α after continuous blood purification therapy in the patients treated with continuous blood purification therapy compared with control group. Conclusion Our study conducted in vivo and in vitro demonstrated that the continuous blood purification therapy could ameliorate the inflammatory response via activating the p38MAPK signaling pathway.

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Section: Discussionmentioning

confidence: 85%

The effect of continuous blood purification on P38MAPK signaling pathway in patients with multiple organ dysfunction syndrome

Pan

2019

Clinical Laboratory Analysis

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“…[21,22]. It has been reported that the p38 MAPK signaling pathway is involved in the inflammatory response and mediates the production of many cytokines, including IL-1β, TNF-α and IL-6 in ARDS [23,24]. Many anti-inflammatory drugs act by targeting p38 MAPK [25].…”

Section: Discussionmentioning

confidence: 99%

miR-128-3p enhances the protective effect of dexmedetomidine on acute lung injury in septic mice by targeted inhibition of MAPK14

Ding

Gao

et al. 2020

Preprint

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Background: To investigate the mechanism of miR-128-3p and MAPK14 on the protective effect of dexmedetomidine on acute lung injury in septic mice. Methods: SPF C57BL/6 mice were divided into 8 groups. The pathological changes and wet/dry weight ratio (W/D), PaO2, PaCO2, MDA, SOD and MPO levels in lung tissue and the serum levels of inflammation factors were observed. Dual luciferase reporter assay was used to verify the targeting relationship between miR-128-3p and MAPK14. qPCR and WB were used to detect the expression of miR-128-3p and MAPK14. Results: Compared with the Normal group, other groups had lower MDA, MPO, inflammatory factors levels and the expression level of MAPK14, while the content of SOD and the expression level of miR-128-3p was significantly decreased. DEX treatment and up-regulation of miR-128-3p could significantly decrease the contents of MDA, MPO, inflammatory factor levels and significantly increase the SOD content in model mice, however, MAPK14 over-expression had opposite effects. miR-128-3p up-regulation enhanced the changes of above indicators caused by DEX treatment and MAPK14 over-expression could block the protective effect of DEX on acute lung injury in septic mice. miR-128-3p up-regulation reversed the effects of MAPK14 over-expression in model mice. Conclusion: miR-128-3p can further enhance the protective effect of dexmedetomidine on acute lung injury in septic mice by targeting and inhibiting MAPK14 expression.

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“…İntestinal İ/R hasarı ince bağırsak dokusunun yanısıra akciğer, karaciğer ve böbrek gibi uzak organlarda hasara neden olmaktadır (6,7). İntestinal İ/R ile oluşan akciğer hasarı reperfüze iskemik bağırsak dokusundan salınan bakteri kökenli endotoksinler ve proinflamatuar sitokinlerin salınımı ile tetiklenmektedir.…”

Section: Discussionunclassified

“…Akut akciğer hasarı olduğunda inflamatuar reaksiyonlar akciğer epitelyumunu harap ederek kapiller permeabilite artışı ve sonuçta pulmoner ödeme neden olmaktadır. Böylece inflamasyon ve pulmoner ödem akut akciğer hasarında iki önemli patolojik karakteristik özelliktir (6,18). Ayrıca salınan inflamatuar mediatörlerle ortaya çıkan SOR akciğer dokusunun endotelyal ve epitelyal hasarında rol oynamaktadır (1,19).…”

Section: Discussionunclassified

“…İ/R mukozal bariyer fonksiyonunu bozarak mukozal ve vasküler permeabilite artışı, bakteriyel translokasyon ve sonuçta sistemik inflamatuar cevap ve çoklu organ yetmezliğine neden olmaktadır (3,4). Çeşitli inflamatuar ve oksidatif mediatörler intestinal İ/R sonrası sistemik dolaşıma salınmakta ve akut akciğer hasarına neden olmaktadır (1,5,6). İntestinal İ/R sonrası akciğer hasarı ve inflamatuar mediatörlerin artışı ile birlikte gözlenmektedir (7).…”

Section: Introductionunclassified

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İntestinal İskemi/Reperfüzyon Modelinde Tiroid Hormon Ön Koşullanmasının İnce Bağırsak Ve Akciğer Hasarı Üzerine Etkisi

TURAN¹,

Özaçmak²,

Barut³

et al. 2017

MJWBS

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Administration of SB239063, a potent p38 MAPK inhibitor, alleviates acute lung injury induced by intestinal ischemia reperfusion in rats associated with AQP4 downregulation

Cited by 41 publications

References 47 publications

The effect of continuous blood purification on P38MAPK signaling pathway in patients with multiple organ dysfunction syndrome

The effect of continuous blood purification on P38MAPK signaling pathway in patients with multiple organ dysfunction syndrome

miR-128-3p enhances the protective effect of dexmedetomidine on acute lung injury in septic mice by targeted inhibition of MAPK14

İntestinal İskemi/Reperfüzyon Modelinde Tiroid Hormon Ön Koşullanmasının İnce Bağırsak Ve Akciğer Hasarı Üzerine Etkisi

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