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Regulation of RhoA/ROCK1 signaling pathway by miR 26b in sepsis induced acute lung injury

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Purpose: To investigate the role of miR-26b in the regulation of RhoA/ ROCK1 signaling pathway in acute lung injury (ALI) caused by sepsis. Methods: Thirty male rats were randomized into sham group (SG), cecal ligation and puncture (CLP) group (CG) and miR-26b mimic group (MG). Hematoxylin and eosin (H & E) staining assay was performed to determine the pathological characteristics of rat lung tissues in each group, while enzyme-linked immunosorbent assay (ELISA) was conducted to determine TNF-α and IL-1β levels. The miR-26b expression was evaluated by quantitative reverse transcription polymerase chain reaction (qRT-PCR), while RhoA and Rock1 protein levels were assessed using western blotting. Results: The CG had significant lung injury in comparison with the SG. There were significant elevation in TNF-α and IL-1β levels (p < 0.05). RhoA and ROCK1 levels in lung tissue were noticeably elevated in CG (p < 0.05). After treatment, lung injury in MG was reduced in contrast to CG. The MG showed statistically significant decrease (p < 0.05) in the levels of TNF-α and IL-1β, while the lung tissue mRNA expression and the RhoA and ROCK1 expression levels were significantly reduced in MG (p < 0.05). Conclusion: The MiR-26b mimics plays an important role in the treatment of ALI induced by sepsis in rats by regulating RhoA/ROCK1 signaling pathway. Thus, the findings of this study provide a theoretical basis for clinical studies on the use of miR-26b in the therapy of sepsis.
Title: Regulation of RhoA/ROCK1 signaling pathway by miR 26b in sepsis induced acute lung injury
Description:
Purpose: To investigate the role of miR-26b in the regulation of RhoA/ ROCK1 signaling pathway in acute lung injury (ALI) caused by sepsis.
Methods: Thirty male rats were randomized into sham group (SG), cecal ligation and puncture (CLP) group (CG) and miR-26b mimic group (MG).
Hematoxylin and eosin (H & E) staining assay was performed to determine the pathological characteristics of rat lung tissues in each group, while enzyme-linked immunosorbent assay (ELISA) was conducted to determine TNF-α and IL-1β levels.
The miR-26b expression was evaluated by quantitative reverse transcription polymerase chain reaction (qRT-PCR), while RhoA and Rock1 protein levels were assessed using western blotting.
Results: The CG had significant lung injury in comparison with the SG.
There were significant elevation in TNF-α and IL-1β levels (p < 0.
05).
RhoA and ROCK1 levels in lung tissue were noticeably elevated in CG (p < 0.
05).
After treatment, lung injury in MG was reduced in contrast to CG.
The MG showed statistically significant decrease (p < 0.
05) in the levels of TNF-α and IL-1β, while the lung tissue mRNA expression and the RhoA and ROCK1 expression levels were significantly reduced in MG (p < 0.
05).
Conclusion: The MiR-26b mimics plays an important role in the treatment of ALI induced by sepsis in rats by regulating RhoA/ROCK1 signaling pathway.
Thus, the findings of this study provide a theoretical basis for clinical studies on the use of miR-26b in the therapy of sepsis.

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