Preventing effects of Pen Yan Jing Tablets on sequelae of pelvic inflammatory disease by inhibiting Akt/NF-κB pathway

Abstract Background: Pen Yan Jing tablets (PYJ), a Chinese patent medicine, has been used for sequelae of pelvic inflammatory disease (SPID) effectively. However, the underlying anti-SPID mechanisms of PYJ remain unknown. The Akt/NF-κB pathway plays an important role in promoting inflammation. This study was designed to investigate whether PYJ has preventing effects on SPID by inhibiting Akt/NF-κB pathway.Methods: A rat model of mixed bacteria liquid plus mechanical damage-induced SPID and a cell model of lipopolysaccharide (LPS)-activated RAW 264.7 macrophages were performed. 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 identified by immunohistochemistry. Additionally, the viability and NO level of lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages were calculated by CCK-8 and Griess method, respectively. The tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels were detected by ELISA. Protein kinase B (Akt)/nuclear factor kappa-B (NF-κB) pathway-related protein expressions were assayed by western blot. Results: PYJ not only remarkably alleviated morphological changes of uteri, pelvic adhesion and histological change of chronic inflammation in uteri, but also down-regulated protein expressions of ICAM-1, VCAM-1, MCP-1, COX-2, p-Akt, p65, p-p65 and p-IκBα in uteri. Moreover, PYJ medicated serum inhibited cell viability, NO release, levels of TNF-α and IL-6, and protein expressions of p-Akt, p-p65 and p-IκBα in LPS-activated RAW 264.7 macrophages. Conclusion: Taken together, the preventing effect of PYJ on SPID attributes to the anti-inflammatory activity via inhibiting Akt/NF-κB pathway.