Abstract
In this study, a knee osteoarthritis (KOA) rat model induced by monosodium iodoacetate (MIA) was used to study the effect of moxibustion on improving knee cartilage damage and its effect on the intestinal flora. The experimental rats were divided into the normal group (N), model group (M), moxibustion treatment group (MS), and diclofenac sodium treatment group (DS). After 4 weeks, cartilage pathological damage in the knee joint was evaluated using hematoxylin-eosin and safranin O-fast green staining analysis. ELISAs and Western blots were used to detect the expression levels of IL-1β and TNF-α in the serum and cartilage, respectively. The total DNA of the fecal samples was extracted and subjected to high-throughput sequencing of the V3-V4 region of the 16S rRNA gene to analyze the changes in the intestinal flora. In the model group, the cartilage was obviously damaged, the expression levels of IL-1β and TNF-α in the serum and cartilage were increased, and the abundance and diversity of the intestinal flora were decreased. Moxibustion treatment significantly improved the cartilage damage and reduced the concentration of inflammatory factors in the serum and cartilage. The high-throughput sequencing results showed that compared to the model group, the moxibustion treatment regulated some specific species in the intestinal microorganisms rather than the α diversity. In conclusion, our findings suggest that moxibustion treatment may work through two aspects in rats. On one hand, it directly acts on knee cartilage to promote repair, and on the other hand, it regulates the composition of the intestinal flora and reduces the production of inflammatory factors.
Highlights
Knee osteoarthritis (KOA) is one of the most common joint diseases, and one-third of people over 65 years old in China suffer from it according to epidemiological surveys [1]
Local tissue damage caused by obesity, advanced age, and genetics can produce a large quantity of damage-associated molecular patterns (DAMPs), which can increase the production of inflammatory factors in the cartilage of the knee joint through various inflammation-promoting effects. e increased inflammatory factors, which cause a chronic continuous lowgrade systemic inflammatory environment, directly induce cartilage catabolism, leading to the failure of cartilage tissue repair and inflammation cycle and to cartilage loss and degeneration [3]
When there was no significant change in the cartilage of the knee joint in the control group and the group injected with monosodium iodoacetate (MIA) showed destruction of the cartilage surface, abnormal safranin O staining, and Mankin score of 4–7 points, the cartilage of the knee joint met the standard of moderate knee osteoarthritis, and the KOA rat model was successfully constructed [12]
Summary
Knee osteoarthritis (KOA) is one of the most common joint diseases, and one-third of people over 65 years old in China suffer from it according to epidemiological surveys [1]. KOA is generally considered to be a kind of degenerative cartilage damage, which has gradually been realized to be caused by chronic low-grade inflammation as the understanding of the disease has increased in the past decade [2]. Local tissue damage caused by obesity, advanced age, and genetics can produce a large quantity of damage-associated molecular patterns (DAMPs), which can increase the production of inflammatory factors (such as interleukin-1β and tumor necrosis factor-α) in the cartilage of the knee joint through various inflammation-promoting effects. Recent research [5] has shown that the emergence and development of systemic chronic low-grade inflammation is closely associated with the intestinal flora, and the composition of which may directly affect lipopolysaccharide (LPS) content to affect the innate immune system.
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