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. 2021 Mar 31:16:877-885.
doi: 10.2147/COPD.S295329. eCollection 2021.

The Mechanism of Penehyclidine Hydrochloride and Its Effect on the Inflammatory Response of Lung Tissue in Rats with Chronic Obstructive Pulmonary Disease During Mechanical Ventilation

Zhi-Yuan Chen  1 , Yi Zhang  1 , Jian-Hua Wu  1 , Xiao-Hua Gao  1 , Chun-Ling Huang  2 , Yu-Mei Lin  1 , Xiao-Ting Xu  1 , Yan Li  1
Affiliations

The Mechanism of Penehyclidine Hydrochloride and Its Effect on the Inflammatory Response of Lung Tissue in Rats with Chronic Obstructive Pulmonary Disease During Mechanical Ventilation

Zhi-Yuan Chen et al. Int J Chron Obstruct Pulmon Dis. .

Retraction in

Abstract

Background: Penehyclidine hydrochloride is a selective antagonist of M1 and M3 receptors. Clinical studies suggest that it is a potential drug for the treatment of chronic obstructive pulmonary disease (COPD). The purpose of this study was to evaluate the effect of penehyclidine hydrochloride on the inflammatory response of lung tissue during mechanical ventilation in rats with COPD and explore the role of the c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) signaling pathway.

Methods: Eight-week-old male Sprague Dawley rats were exposed to cigarette smoke for 30 minutes every day for two months, and on the first and thirtieth days, 200 ug of lipopolysaccharide was injected into the trachea. Two months later, the rats were randomly divided into the control group (C), model group (M), model + normal saline group (N), and penehyclidine hydrochloride group (H) to undergo anesthesia and mechanical ventilation. In group H, 1 mg/kg of penehyclidine hydrochloride was injected intravenously.

Results: The results showed that: ① Compared with group C, the other groups all showed typical chronic obstructive pathological changes in the lung tissue; their wet/dry weight ratio (W/D), TNF-α, JNK, and p-JNK levels increased (P < 0.05), and their interleukin (IL)-10 levels decreased (P < 0.05). ② Compared with group M, there was no significant change in the lung tissue indexes in group N (P > 0.05). ③ Compared with group N, the W/D, TNF-α, JNK, and p-JNK levels in group H decreased (P < 0.05), while the levels of IL-10 increased (P < 0.05).

Conclusion: Penehyclidine hydrochloride can alleviate the pulmonary inflammatory response in rats with COPD undergoing mechanical ventilation. The JNK/SAPK signaling pathway may be involved in this process.

Keywords: IL-10; JNK; TNF-α; chronic obstructive pulmonary disease; p-JNK; penehyclidine hydrochloride.

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Conflict of interest statement

The authors report no conflicts of interest in this work.

Figures

Figure 1
Figure 1
(A) Pathological section image of the lung tissue of rats in control group (C) (HE staining × 200). (B) Pathological section image of the lung tissue of rats in model group (M) (HE staining × 200). (C) Pathological section image of the lung tissue of rats in model + normal saline group (N) (HE staining × 200). (D) Pathological section image of the lung tissue of rats in penehyclidine hydrochloride group (H) (HE staining × 200).
Figure 2
Figure 2
Comparison of the W/D, TNF-α, and IL-10 levels in the lung tissue of rats in each group (n = 12, X ± s).
Figure 3
Figure 3
Comparison of JNK and p-JNK levels in the lung tissue of rats in each group (n = 12, X ± s).
Figure 4
Figure 4
Expression of JNK and p-JNK in the lung tissue of rats in each group detected by Western blotting.
See this image and copyright information in PMC

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