Acute lung injury (ALI) is an acute hypoxic respiratory insufficiency caused by various intra- and extrapulmonary injury factors. Presently, excessive inflammation in the lung and the apoptosis of alveolar epithelial cells are considered to be the key factors in the pathogenesis of ALI. Hypoxia-inducible factor-1 (HIF-1) is an oxygen-dependent conversion activator that is closely related to the activity of reactive oxygen species (ROS). HIF-1 has been shown to play an important role in ALI and can be used as a potential therapeutic target for ALI. This manuscript will introduce the progress of HIF-1 in ALI and explore the feasibility of applying inhibitors of HIF-1 to ALI, which brings hope for the treatment of ALI.

/pdf/hypoxia-inducible-factor-1-a-potential-target-to-treat-acute-3ixe4jhyuf.pdf

Hypoxia-Inducible Factor-1: A Potential Target to Treat Acute Lung Injury.

Effects of penehyclidine hydrochloride on severe acute pancreatitis-associated acute lung injury in rats.

Ischemic heart disease is a major cause of mortality and disability worldwide. Timely reperfusion is currently the most effective method of treating ischemic heart disease; however, abrupt reperfusion may cause ischemia/reperfusion (I/R) injury. Apoptosis serves an important role in the progression of myocardial I/R injury and it has been demonstrated that the mitochondria are the center of regulation for apoptosis. Penehyclidine hydrochloride (PHC) is used during surgery and has recently been identified as a new type of anticholinergic drug. It has been demonstrated in vivo that pretreatment with PHC reduces myocardial apoptosis in rat hearts. The present study aimed to investigate the effects of PHC post-conditioning on myocardial cell apoptosis in a rat model of myocardial I/R and to determine whether the mitochondria-induced pathway was activated. Male Wistar rats were evenly and randomly categorized into 4 experimental groups as follows: i) Sham group; ii) I/R group; iii) PHC+sham group; and iv) PHC+I/R group. A PHC (1 mg/kg) post-conditioning approach (5 min before reperfusion) was used in addition to I/R in the PHC-treated groups. Following 3 h reperfusion, flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling staining were performed to measure myocardial cell apoptosis. A JC-1 staining method was performed to measure the mitochondrial membrane potential of myocardial cells. The expression of Bax, Bcl-2, voltage dependent anion-selective channel protein 1 (VDAC1), cytosol cytochrome c (cyt-c) and cleaved caspase-3 was analyzed using western blotting. PHC post-conditioning significantly reduced apoptosis in cardiomyocytes, significantly downregulated the expression of Bax, VDAC1, cytosol cytochrome c and cleaved caspase-3 but significantly upregulated the expression of Bcl-2. PHC post-conditioning also restored the mitochondrial membrane potential. Thus, the present study demonstrated that PHC post-conditioning protects cardiomyocytes against apoptosis in the rat model of myocardial I/R by inhibiting the mitochondria-induced intrinsic pathway.

/pdf/penehyclidine-hydrochloride-post-conditioning-reduces-1nza7fdrwx.pdf

Penehyclidine hydrochloride post-conditioning reduces ischemia/reperfusion-induced cardiomyocyte apoptosis in rats.

We aimed to observe the effect of penehyclidine hydrochloride (PHC) on lipopolysaccharide (LPS)-induced acute kidney injury in rats and expression of tight junction proteins ZO-1 and occludin. Adult male Sprague-Dawley (SD) rats were divided randomly (N = 10) into control group (C), LPS group (LPS), low-dose PHC group (L-PHC), and high-dose PHC group (H-PHC). All rats, except C group, received a vena caudalis injection of 5.0 mg/kg LPS; after 30 min, rats in L-PHC and H-PHC groups received a vena caudalis injection of 0.3 and 0.9 mg/kg PHC. After 24 h, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, serum creatinine (Scr), and blood urea nitrogen (BUN) were detected. Histopathological changes and expression of ZO-1 and occludin were observed in renal tissues. Versus levels of TNF-α (38.5 ± 9.0), IL-1β (46.3 ± 12.7), Scr (37.2 ± 9.3), and BUN (6.5 ± 1.1) in control group, those in LPS group, TNF-α (159.0 ± 21.3), IL-1β (130.8 ± 18.7), Scr (98.5 ± 18.2), and BUN (12.8 ± 1.8), increased obviously (P < 0.05), with significantly structural changes and decreases of ZO-1 and occludin. However, TNF-α (111.3 ± 11.6), IL-1β (78.4 ± 14.3), Scr (51.3 ± 12.5), BUN (8.1 ± 1.2) in H-PHC group, and TNF-α (120.8 ± 14.3), IL-1β (92.5 ± 19.0), Scr (56.7 ± 14.7), BUN (9.7 ± 1.6) in L-PHC group were obviously decreased (P < 0.05). PHC has protective effects on acute kidney injury in sepsis, including abatement of renal tissue inflammation and functional improvement, potentially by upregulating ZO-1 and occludin.

/pdf/protective-effect-of-penehyclidine-hydrochloride-on-34194e8wp2.pdf

Protective effect of penehyclidine hydrochloride on lipopolysaccharide-induced acute kidney injury in rat.

Cardioprotective time-window of Penehyclidine hydrochloride postconditioning: A rat study

Penehyclidine hydrochloride decreases pulmonary microvascular permeability by upregulating beta arrestins in a murine cecal ligation and puncture model.

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Penehyclidine hydrochloride decreases pulmonary microvascular permeability by upregulating beta arrestins in a murine cecal ligation and puncture model.