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Pen Yan Jing Tablets Alleviates Pelvic Inflammatory Disease by Inhibiting Akt/NF-κB Pathway

Purpose: Pen Yan Jing tablets (PYJ), a Chinese patent medicine, has being used for pelvic inflammatory disease (PID) effectively. This study was designed to explore the underlying mechanisms of PYJ for treating PID. Methods: A rat model of PID was established by mixed bacteria liquid plus mechanical...

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Autores principales: Tang, Ping, Ding, Qi, Lin, Juan, Yang, Xinrong, Wang, Yiting, Liu, Fangle, Zheng, Yuying, Lin, Liuqing, Wang, Deqin, Lin, Baoqin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10542183/
https://www.ncbi.nlm.nih.gov/pubmed/37790843
http://dx.doi.org/10.7150/ijms.87433
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author Tang, Ping
Ding, Qi
Lin, Juan
Yang, Xinrong
Wang, Yiting
Liu, Fangle
Zheng, Yuying
Lin, Liuqing
Wang, Deqin
Lin, Baoqin
author_facet Tang, Ping
Ding, Qi
Lin, Juan
Yang, Xinrong
Wang, Yiting
Liu, Fangle
Zheng, Yuying
Lin, Liuqing
Wang, Deqin
Lin, Baoqin
author_sort Tang, Ping
collection PubMed
description Purpose: Pen Yan Jing tablets (PYJ), a Chinese patent medicine, has being used for pelvic inflammatory disease (PID) effectively. This study was designed to explore the underlying mechanisms of PYJ for treating PID. Methods: A rat model of PID was established by mixed bacteria liquid plus mechanical damage. After PYJ treatment, the morphology of uteri and extent of pelvic adhesion were observed. The pathological changes were evaluated by hematoxylin-eosin (HE) staining. The protein expressions of CD68, intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), monocyte chemotactic protein-1 (MCP-1) and cyclooxygenase-2 (COX-2) were quantitated by immunohistochemistry. A cell model of lipopolysaccharide (LPS)-activated RAW 264.7 macrophages was performed. The cell proliferation and NO level were measured by CCK-8 and Griess method, respectively. The tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels were detected by ELISA. The protein kinase B (Akt)/nuclear factor kappa-B (NF-κB) pathway-related protein expressions were assayed by western blot or immunofluorescence. Results: PYJ alleviated pelvic adhesion and inflammatory lesions of uteri in PID rats. PYJ down-regulated protein expressions of ICAM-1, VCAM-1, MCP-1, COX-2, p-Akt, p-IκB kinaseα/β (p-IKKα/β), p-IκBα, p65, and p-p65 in uteri of PID rats. Moreover, PYJ medicated serum inhibited abnormal cell proliferation, NO release, levels of TNF-α and IL-6, nuclear translocation of p65, and protein expressions of p-Akt, p-p65 and p-IκBα in LPS-activated RAW 264.7 macrophages. Conclusions: Taken together, PYJ may alleviates PID through inhibiting Akt/NF-κB pathway.
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spelling pubmed-105421832023-10-03 Pen Yan Jing Tablets Alleviates Pelvic Inflammatory Disease by Inhibiting Akt/NF-κB Pathway Tang, Ping Ding, Qi Lin, Juan Yang, Xinrong Wang, Yiting Liu, Fangle Zheng, Yuying Lin, Liuqing Wang, Deqin Lin, Baoqin Int J Med Sci Research Paper Purpose: Pen Yan Jing tablets (PYJ), a Chinese patent medicine, has being used for pelvic inflammatory disease (PID) effectively. This study was designed to explore the underlying mechanisms of PYJ for treating PID. Methods: A rat model of PID was established by mixed bacteria liquid plus mechanical damage. After PYJ treatment, the morphology of uteri and extent of pelvic adhesion were observed. The pathological changes were evaluated by hematoxylin-eosin (HE) staining. The protein expressions of CD68, intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), monocyte chemotactic protein-1 (MCP-1) and cyclooxygenase-2 (COX-2) were quantitated by immunohistochemistry. A cell model of lipopolysaccharide (LPS)-activated RAW 264.7 macrophages was performed. The cell proliferation and NO level were measured by CCK-8 and Griess method, respectively. The tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels were detected by ELISA. The protein kinase B (Akt)/nuclear factor kappa-B (NF-κB) pathway-related protein expressions were assayed by western blot or immunofluorescence. Results: PYJ alleviated pelvic adhesion and inflammatory lesions of uteri in PID rats. PYJ down-regulated protein expressions of ICAM-1, VCAM-1, MCP-1, COX-2, p-Akt, p-IκB kinaseα/β (p-IKKα/β), p-IκBα, p65, and p-p65 in uteri of PID rats. Moreover, PYJ medicated serum inhibited abnormal cell proliferation, NO release, levels of TNF-α and IL-6, nuclear translocation of p65, and protein expressions of p-Akt, p-p65 and p-IκBα in LPS-activated RAW 264.7 macrophages. Conclusions: Taken together, PYJ may alleviates PID through inhibiting Akt/NF-κB pathway. Ivyspring International Publisher 2023-09-04 /pmc/articles/PMC10542183/ /pubmed/37790843 http://dx.doi.org/10.7150/ijms.87433 Text en © The author(s) https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Research Paper
Tang, Ping
Ding, Qi
Lin, Juan
Yang, Xinrong
Wang, Yiting
Liu, Fangle
Zheng, Yuying
Lin, Liuqing
Wang, Deqin
Lin, Baoqin
Pen Yan Jing Tablets Alleviates Pelvic Inflammatory Disease by Inhibiting Akt/NF-κB Pathway
title Pen Yan Jing Tablets Alleviates Pelvic Inflammatory Disease by Inhibiting Akt/NF-κB Pathway
title_full Pen Yan Jing Tablets Alleviates Pelvic Inflammatory Disease by Inhibiting Akt/NF-κB Pathway
title_fullStr Pen Yan Jing Tablets Alleviates Pelvic Inflammatory Disease by Inhibiting Akt/NF-κB Pathway
title_full_unstemmed Pen Yan Jing Tablets Alleviates Pelvic Inflammatory Disease by Inhibiting Akt/NF-κB Pathway
title_short Pen Yan Jing Tablets Alleviates Pelvic Inflammatory Disease by Inhibiting Akt/NF-κB Pathway
title_sort pen yan jing tablets alleviates pelvic inflammatory disease by inhibiting akt/nf-κb pathway
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10542183/
https://www.ncbi.nlm.nih.gov/pubmed/37790843
http://dx.doi.org/10.7150/ijms.87433
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