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Purpose: Mitochondrial dysfunction of chondrocytes has become an area of focus in Knee Osteoarthritis (KOA) in recent years. Activation of mitophagy could promote the survival of chondrocytes and alleviate cartilage degeneration. The aim of this study was to explore whether mitophagy was involved in the cartilage protection of KOA rabbits after electroacupuncture (EA) intervention. Methods: The rabbits were divided into 3 groups, Control group, KOA group, EA group, with 6 rabbits in each group. KOA model rabbits were established by modified Videman's extended immobilization method for 6 weeks and randomly divided into KOA group and EA group. The rabbits in EA group were treated every other day for 3 weeks. The degree of cartilage degeneration was detected by Safranine O-Fast Green staining and immunofluorescence. The morphological changes of chondrocytes mitochondria were detected by transmission electron microscope. ATP concentration in cartilage was measured by ATP Assay Kit. The changes of Pink1-Parkin signal pathway were detected by immunofluorescence, Western blot, and Real-time PCR. Results: The morphology showed that EA could reduce the degeneration of KOA cartilage and increase the distribution of collagen II. We also found that EA could activate mitophagy in KOA rabbit chondrocytes to remove damaged mitochondria and restore mitochondrial homeostasis, which was manifested as increasing the expression of LC3 II/I, promoting the colocalization of TOM20 and LC3B, reducing the accumulation of mitochondrial markers outer mitochondrial membrane 20 (TOM20) and inner mitochondrial membrane 23 (TIM23), and increasing ATP production in chondrocytes. This regulation might be achieved by upregulating the Pink1-Parkin signal pathway. Conclusion: EA may play a role in protecting KOA cartilage by activating mitophagy mediated through Pink1-Parkin pathway.
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Purpose: Knee osteoarthritis (KOA) is a chronic inflammatory disease highly associated with intra-articular hypertension, hypoxia and angiogenesis of synovial tissue. Our previous studies showed that acupotomy could treat KOA in a variety of ways, including reducing cartilage deterioration and enhancing biomechanical qualities. However, the mechanism of hypoxia and angiogenesis induced by acupotomy in KOA synovium remains unclear. This study looked for the benign intervention of acupotomy in synovial pathology. Methods: The rabbits were divided into 3 groups, Normal group, KOA group, and KOA + Acupotomy (Apo) group, with 11 rabbits in each group. The KOA rabbit model was established by the modified Videman method with six weeks. The KOA + Apo group performed the intervention. The tendon insertion of vastus medialis, vastus lateralis, rectus femoris, biceps femoris, and anserine bursa were selected as treatment points in rabbits. Rabbits were treated once every 7 days for 3 weeks. We observed the intra-articular pressure and oxygen partial pressure (BOLD MRI). The synovial morphology was monitored by Hematoxylin-Eosin Staining (HE Staining). The expression of hypoxia-inducible transcription factor-1α (HIF-1α), vascular endothelial growth factor (VEGF), interleukin-1ß (IL-1ß) and tumour necrosis factor-α (TNF-α) was detected using Immunohistochemical (IHC), Western Blot and Enzyme-Linked Immunosorbent Assay (ELISA). Results: Acupotomy reduced intra-articular hypertension and improved the synovial oxygen situation, synovial inflammatory and angiogenesis. HIF-1α, VEGF, IL-1ß and TNF-α expression were downregulated by acupotomy. Conclusion: Acupotomy may reduce inflammation and angiogenesis in KOA rabbit by reducing abnormally elevated intra-articular pressure and improving synovial oxygen environment. The above may provide a new theoretical foundation for acupotomy treatment of KOA.
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BACKGROUND: Increasing attention has been paid to the potential relationship between gut and lung. The bacterial dysbiosis in respiratory tract and intestinal tract is related to inflammatory response and the progress of lung diseases, and the pulmonary diseases could be improved by regulating the intestinal microbiome. This study aims to generate the knowledge map to identify major the research hotspots and frontier areas in the field of gut-lung axis. MATERIALS AND METHODS: Publications related to the gut-lung axis from 2011 to 2021 were identified from the Web of Science Core Collection. CiteSpace 5.7.R2 software was used to analyze the publication years, journals, countries, institutions, and authors. Reference co-citation network has been plotted, and the keywords were used to analyze the research hotspots and trends. RESULTS: A total of 3315 publications were retrieved and the number of publications per year increased over time. Our results showed that Plos One (91 articles) was the most active journal and The United States (1035 articles) published the most articles. We also observed the leading institution was the University of Michigan (48 articles) and Huffnagle Gary B, Dickson Robert P and Hansbro Philip M, who have made outstanding contributions in this field. CONCLUSION: The Inflammation, Infection and Disease were the hotspots, and the regulation of intestinal flora to improve the efficacy of immunotherapy in lung cancer was the research frontier. The research has implications for researchers engaged in gut-lung axis and its associated fields.
