PHARMACOLOGICAL STUDY OF PROTECTIVE EFFECT OF THYMOQUINONE IN A MODEL OF LUNG INJURY

2012 ◽  
Vol 45 (1) ◽  
pp. 74-85
Author(s):  
Dalia El-Khouly
2021 ◽  
Vol 49 (2) ◽  
pp. 030006052098635
Author(s):  
Qi Gao ◽  
Ningqing Chang ◽  
Donglian Liu

Objectives To investigate the mechanisms underlying the protective effect of sufentanil against acute lung injury (ALI). Material and Methods Rats were administered lipopolysaccharide (LPS) by endotracheal instillation to establish a model of ALI. LPS was used to stimulate BEAS-2B cells. The targets and promoter activities of IκB were assessed using a luciferase reporter assay. Apoptosis of BEAS-2B cells was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling. Results Sufentanil treatment markedly reduced pathological changes in lung tissue, pulmonary edema and secretion of inflammatory factors associated with ALI in vivo and in vitro. In addition, sufentanil suppressed apoptosis induced by LPS and activated NF-κB both in vivo and in vitro. Furthermore, upregulation of high mobility group box protein 1 (HMGB1) protein levels and downregulation of miR-129-5p levels were observed in vivo and in vitro following sufentanil treatment. miR-129-5p targeted the 3ʹ untranslated region and its inhibition decreased promoter activities of IκB-α. miR-129-5p inhibition significantly weakened the protective effect of sufentanil on LPS-treated BEAS-2B cells. Conclusion Sufentanil regulated the miR-129-5p/HMGB1 axis to enhance IκB-α expression, suggesting that sufentanil represents a candidate drug for ALI protection and providing avenues for clinical treatment.


2014 ◽  
Vol 59 (9) ◽  
pp. 1412-1421 ◽  
Author(s):  
T. Li ◽  
S. Cai ◽  
Z. Zeng ◽  
J. Zhang ◽  
Y. Gao ◽  
...  

2018 ◽  
Vol 120 (3) ◽  
pp. 3323-3330 ◽  
Author(s):  
Heyuan Wang ◽  
Wei Wu ◽  
Guixia Wang ◽  
Wenzhou Xu ◽  
Fuqiang Zhang ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Haifa Xia ◽  
Jingxu Wang ◽  
Shujun Sun ◽  
Fuquan Wang ◽  
Yiyi Yang ◽  
...  

As one of the basic treatment modalities in the intensive care unit (ICU), mechanical ventilation can cause or aggravate acute lung injury or ventilator-induced lung injury (VILI). Resolvin D1 (RvD1) is an endogenous polyunsaturated fatty acid derivative with strong anti-inflammatory action. In this study, we explored if RvD1 possesses a protective effect on VILI. Mice were ventilated with high tidal volume (40 mL/kg, HVT) for 4 h and were then intraperitoneally administered RvD1 at the beginning of high tidal volume ventilation and given GW9662 (a PPAR-γ antagonist) intraperitoneally 30 min before ventilation. RvD1 attenuated VILI, as evidenced by improved oxygenation and reduced histological injury, compared with HVT -induced lung injury. Similarly, it could ameliorate neutrophil accumulation and production of proinflammatory cytokines in lung tissue. In contrast, the protective effect of RvD1 on lung tissue could be reversed by GW9662. RvD1 mitigated VILI by activating peroxisome proliferator-activated receptor gamma (PPAR-γ) and inhibiting nuclear factor-kappa B (NF-κB) signaling pathways in mice. In conclusion, RvD1 could reduce the inflammatory response in VILI by activating PPAR-γ and inhibiting NF-κB signaling pathways.


2014 ◽  
Vol 239 (12) ◽  
pp. 1653-1662 ◽  
Author(s):  
Lian Wang ◽  
Jinming Chen ◽  
Bo Wang ◽  
Dingqian Wu ◽  
Hao Li ◽  
...  

Author(s):  
Hung Chang ◽  
Yu-Chien Kung ◽  
Shih-Chun Lee ◽  
Chung-Cheng Kao ◽  
Chia-Yu Chang ◽  
...  

2015 ◽  
Vol 25 (1) ◽  
pp. 55-64 ◽  
Author(s):  
Tong Chen ◽  
Yi Mou ◽  
Jiani Tan ◽  
Linlin Wei ◽  
Yixue Qiao ◽  
...  

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