The effectiveness of smokeless moxa and other means to reduce exposure are extensively investigated with regards to the health consequences of inhalation of moxa smoke, and clinical studies indicate that classical moxibustion is superior to smokeless moxa. This study aims to quantify the effects of particle density in moxa smoke on the clinical outcome with an established model, demonstrated to be effective for classical moxibustion.
The purpose of this study is to explore the effects of particle density in moxa smoke on the ultrastructure of knee cartilage and expression of cytokine, tissue necrosing factor-alpha (TNF-α), interleukin 1 beta (IL-1b), apoptosis regulator, B-cell lymphoma-2 (Bcl-2), and BAX in a rat model for inflammatory joint disease.
Fifty healthy experimental rats were randomly divided into five groups, including normal control, model control, and moxa exposure groups with low, medium, and high particle density, and n = 10/group. In addition, a knee osteoarthritis model was duplicated in the model control and moxa exposure groups. Finally, the ultrastructure of knee cartilage was observed using transmission electron microscopy, and messenger RNA (mRNA) expressions of TNF-α, IL-1b, BAX, and Bcl-2 were determined with quantitative fluorescence methodology.
In the model control and moxa exposure groups, knee cartilage indicated that histologic changes with the degree of injury were inversely proportional to moxa smoke density. The mRNA expressions of TNF-α, IL-1b, and BAX in synovial fluid, as an acute phase reactant, were similarly inversely related to moxa smoke density, but significantly increased. In contrast, Bcl-2, as an antiapoptotic, was substantially decreased in the model, while its levels were directly proportional to moxa smoke density. Besides, the ratio of Bcl-2/BAX mRNA was sharply decreased in the model group, but with levels proportional to moxa smoke density.
A correlation was found between the particle density in moxa smoke and degree of injury to knee cartilage, favoring higher particle densities. This can be partially related to the suppression of the inflammatory effects of TNF-α, IL-1b, enhancement of the antiapoptotic effects of Bcl-2, and, nevertheless, suppression of the apoptotic effects of BAX. Finally, the protective effect of antiapoptotic is one of the key mechanisms for an ambient moxa smoking environment.