1.Chinese Medicine Intervenes in NLRP3 Inflammasome in Treatment of Bone and Joint Diseases: A Review
Tuanzhuang ZHANG ; Yuan SONG ; Zhijun HE ; Tao LIU ; Xiyan LYU ; Xiaotao WEI ; Jiaxuan SHEN ; Xudong LIANG ; Keyu ZHU ; Jing QIAO
Chinese Journal of Experimental Traditional Medical Formulae 2023;29(22):193-203
The prevalence of osteoporosis, osteoarthritis, gouty arthritis, rheumatoid arthritis, and intervertebral disc degeneration is increasing year by year with the growing number of elderly people, and the common clinical manifestations of these diseases include severe pain in different areas, which seriously affects the daily life of the patients. Therefore, how to relieve the pain and reduce the prevalence of bone and joint diseases and improve the quality of life of the patients is a hot spot in the medical field. Studies have confirmed that NOD-like receptor family, pyrin domain-containing protein 3 (NLRP3) inflammasomes, as pattern recognition receptors, are involved in the inflammation, chondrocyte proliferation, osteoblast and osteoclast differentiation, intervertebral disc cell inflammation and scorching, extracellular matrix degradation and apoptosis, mitochondrial dysfunction, endoplasmic reticulum stress, and reactive oxygen species damage, demonstrating close link with the development of bone and joint diseases. Chinese medicine has a long history and demonstrates remarkable therapeutic effects in the treatment of bone and joint diseases. It can mitigate the pathological changes of bone and joint diseases by inhibiting NLRP3 inflammasomes to alleviate the pain, playing a role in preventing and treating these diseases. Therefore, this paper briefly describes the relationship between NLRP3 inflammasomes and the development of bone and joint diseases by reviewing the latest research progress at home and abroad. We summarize the latest studies about the active components, extracts, and compound prescriptions of Chinese medicines in the treatment of bone and joint diseases via regulating NLRP3 inflammasomes. This review is expected to offer new insights into the in-depth research on the pathogenesis and drug treatment of bone and joint diseases and provide a basis for the clinical application of Chinese medicine in the prevention and treatment of such diseases.
2.Effect of Xiaozhongzhitong Mixture on ischemia-reperfusion injury of rat skin flaps and p38MAPK-PPARγ/NF-κB signaling pathway
Yuan SONG ; Haigang WANG ; Zhijun HE ; Tao LIU ; Xudong LIANG ; Yuanxu HE ; Jiaxuan SHEN ; Tuanzhuang ZHANG
Journal of Xi'an Jiaotong University(Medical Sciences) 2023;44(1):126-134
【Objective】 To observe the effect of Xiaozhongzhitong Mixture on ischemia-reperfusion injury of rat skin flaps and p38MAPK-PPARγ/NF-κB signaling pathway. 【Methods】 After flap operation, the survival of rat back flaps and flap survival rate were observed. HE staining, TUNEL staining, and qRT-PCR were used to detect the degree of nuclear destruction, as well as the distribution characteristics and mRNA expression levels of p38MAPK, PPARγ, and Nf-κB in vascular endothelial cells of rat flaps, respectively. 【Results】 The flap survival area in sham operation group was the largest, and it was the smallest in model control group and PPARγ inhibitor group. HE staining and TUNEL staining results showed that the flap tissue cells of rats in model control group and PPARγ inhibitor group were severely damaged and obvious apoptotic cells were seen. In model group, rats’ skin flap tissue cells were arranged in a single layer, and the nucleus was intact and clear. qRT-PCR experiment results showed that compared with model group, the expressions of p38MAPK and Nf-κb in the flap tissue of rats in Xiaozhong Zhicong Mixture group were inhibited (P<0.05), while the expression of PPARγ was increased (P<0.05). When the blocker was added, the expressions of p38MAPK, NF-κB and PPARγ in the flap tissue were further suppressed. 【Conclusion】 Xiaozhongzhitong Mixture can alleviate the infiltration of inflammatory cells in the rat model of skin flap ischemia-reperfusion injury, reduce inflammation and the production of apoptotic cells, thereby alleviating the ischemia-reperfusion injury of skin flaps and promoting the survival of the flaps. The mechanism may be related to the inhibition of p38MAPK-PPARγ/NF-κB signaling pathway.