ArticleMolecular biology reports2011
Effect of penehyclidine hydrochloride on expressions of MAPK in mice with CLP-induced acute lung injury.
Article in Molecular biology reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 25 citations in OpenAlex.
- Prevention of renal ischemia and reperfusion injury by penehyclidine hydrochloride through autophagy activation.Molecular medicine reports · 2020Article
- Smoking Attenuates Efficacy of Penehyclidine Hydrochloride in Acute Respiratory Distress Syndrome Induced by Lipopolysaccharide in Rats.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Activation of multiple Toll-like receptors serves different roles in sepsis-induced acute lung injury.Experimental and therapeutic medicine · 2019Article
- Penehyclidine hydrochloride inhibits TLR4 signaling and inflammation, and attenuates blunt chest trauma and hemorrhagic shock-induced acute lung injury in rats.Molecular medicine reports · 2018Article
- Pleiotropic effects and pharmacological properties of penehyclidine hydrochloride.Drug design, development and therapy · 2018Review
- Anti-inflammatory effects of novel curcumin analogs in experimental acute lung injury.Respiratory research · 2015Article
- Exogenous carbon monoxide attenuates inflammatory responses in the small intestine of septic mice.World journal of gastroenterology · 2012Article
- Penehyclidine hydrochloride attenuates LPS-induced iNOS production by inhibiting p38 MAPK activation in endothelial cells.Molecular biology reports · 2012Article
- Troglitazone-activated PPARγ inhibits LPS-induced lung alveolar type II epithelial cells injuries via TNF-α.Molecular biology reports · 2011Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Penehyclidine hydrochloride (PHC) is a new anticholinergic drug. PHC has been shown to have a good curative effect for sepsis. Mitogen-activated protein kinase (MAPK) has recently been considered to play an important role in sepsis. In this study, the role of MAPK signal pathways in protective effects of PHC preconditioning on acute lung injury in cecal ligation and puncture (CLP)-induced sepsis was investigated. Healthy female mice were randomly divided into 4 groups: sham control, CLP, and 0.3 or 0.45 mg/kg PHC. At 12 h after surgery, arterial blood was drawn for blood gas analysis, and lung tissue samples were collected to examine pulmonary microvascular permeability, IL-6 levels and myeloperoxidase (MPO) activity. MAPK protein expressions were measured using western blot technique. Compared with sham control mice, acute lung injury was induced in CLP group, which was indicated by decreased PaO(2)/FiO(2), increased pulmonary microvascular permeability, IL-6 levels and MPO activity. Furthermore, mice' exposure to CLP induced the increased protein levels of MAPK. Treatment of 0.45 mg/kg PHC markedly improved PaO(2)/FiO(2), decreased pulmonary microvascular permeability, IL-6 levels and MPO activity, and inhibited expressions of extracellular signal-regulated kinase (ERK1/2) and p38 MAPK. Taken together, these results suggest that PHC ameliorated acute lung injury through the inhibition of extracellular signal-regulated kinase (ERK1/2) and p38 MAPK activation in septic mice.
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