The Effects of Xiangqing Anodyne Spray on Treating Acute Soft-Tissue Injury Mainly Depend on Suppressing Activations of AKT and p38 Pathways. (14th April 2016)

• Record Type: Journal Article
• Authors: Wang, Shudong; Li, Tao; Qu, Wei; Li, Xin; Ma, Shaoxin; Wang, Zheng; Liu, Wenya; Hou, Shanshan; Fu, Jihua
• Other Names: Oh Ki-Wan Academic Editor.
• Is Part Of: Evidence-based complementary and alternative medicine. Volume 2016(2016)
• Publication Date: 2016-04-14
• Subjects: Alternative medicine -- Periodicals; 615.505
• DOI: 10.1155/2016/9213489
• Languages: English
• ISSNs: 1741-427X

Abstract

Abstract : Objectives . In the present study we try to elucidate the mechanism of Xiangqing anodyne spray (XQAS) effects on acute soft-tissue injury (STI). Methods . Acute STI model was established by hammer blow in the rat hind leg muscle. Within 8 hours, instantly after modeling and per 2-hour interval repeated topical applications with or without XQAS, CP or IH ethanol extracts spray (CPS and IHS) were performed, respectively; muscle swelling rate and inflammation-related biochemical parameters, muscle histological observation, and mRNA and protein expression were then examined. Results . XQAS dose-dependently suppressed STI-caused muscle swelling, proinflammatory mediator productions, and oxidative stress as well as severe pathological changes in the injured muscle tissue. Moreover, CPS mainly by blocking p38 activation while IHS majorly by blocking AKT activation led to cytoplastic I κ B α degradation with NF- κ B p65 translocated into the nucleus. There are synergistic effects between CP and IH components in the XQAS on preventing from acute STI with suppressing I κ B α degradation, NF- κ B p65 translocation, and subsequent inflammation and oxidative stress-related abnormality. Conclusion . Marked effects of XQAS on treating acute STI are ascribed to strong anti-inflammatory and antioxidative actions with a reasonable combination of CP active components, blocking p38-NF- κ B pathway activated, and IH active components, blocking AKT-NF- κ B pathway activated.