RESUMO
Tendon-bone healing is a complex biological process. Multiple signaling pathways are involved in tendon-bone healing， including transforming growth factor-β signaling pathway， bone morphogenetic protein signaling pathway， Wnt signaling pathway， fibroblast growth factor signaling pathway and nuclear transcription factor-κB signaling pathway. This paper summarizes the research status of traditional Chinese medicine regulating related signaling pathways to promote tendon-bone healing. It is found that a variety of traditional Chinese medicine monomers or herbal extracts （such as baicalein， icariin， total flavonoids of Drynaria fortunei， parthenolide， total saponins of Panax notoginseng， etc.） and traditional Chinese medicine compounds （such as Taohong siwu decoction， Liuwei dihuang pill， Xujin jiegu liquid， etc.） can promote bone formation， anti-inflammatory， anti-oxidation， by regulating the above signaling pathways， thereby effectively promoting tendon-bone healing.
RESUMO
Osteoarthritis (OA) is a common chronic degenerative disease, and its condition tends to worsen with age. The pathogenesis of OA is complex, and many risk factors can lead to the occurrence of OA. Iron is one of the essential trace elements in the body, and its metabolic balance is extremely important to human health. Iron overload is closely related to the occurrence and development of OA. Excessive iron deposition in joint tissue can easily lead to lesions of articular cartilage and synovium, as well as affect subchondral bone reconstruction and lead to the occurrence of OA. The author reviewed the relevant research literature in recent years, and reviewed the mechanism of iron overload in the occurrence and development of OA, in order to provide new ideas and directions for the research and diagnosis and treatment of OA.
RESUMO
Background Trichloroethylene (TCE) can enter human body through biological accumulation of polluted water or air, resulting in health hazards. The most commonly involved organs are the liver. Objective To observe potential polarization of M1 Kupffer cells (KCs) in mice liver exposed to TCE orally, and to investigate the relationship between histones lysin demethylase JMJD3 and M1 KCs polarization. Methods A total of 72 SPF BALB/c mice aged 6 to 8 weeks were randomly divided into a blank control group (n=18), a vehicle control group (n=18), a 2.5 mg·mL−1 TCE group (n=18), and a 5.0 mg·mL−1 TCE group (n=18) after adaptive feed for one week. A TCE transoral exposure model was established after eight weeks of administration according to previous research of the research group. In the 2nd, 4th, and 8th weeks, the mice were sacrificed and liver tissue samples were collected. Western blotting was used to detect the expression level of JMJD3 in the liver tissue samples. Immunofluorescence was used to co-locate the macrophage marker F4/80 and the surface marker CD11c of M1 macrophages. Immunohistochemistry was used to detect the expressions of CD16/32, a marker of M1 macrophages, and TNF-α, an inflammatory factor of M1 macrophages in mouse liver. Results In the 2nd, 4th, and 8th weeks, the mice in each group were generally in good condition, and no individual died due to TCE. There was no statistically significant difference in the amount of water consumed by each group, nor in the body weight gain and the liver coefficient of mice at each time point (P>0.05). The results of Western blotting analysis showed that there was no statistically significant difference in JMJD3 protein expression level between the blank control group and the vehicle control group at each time point, the expression levels of JMJD3 protein in the 2.5 mg·mL−1 TCE group and the 5.0 mg·mL−1 TCE group were higher than that in the control group , and the expression level of JMJD3 protein in the 5.0 mg·mL−1 TCE group was higher than that in the 2.5 mg·mL−1 TCE group (P<0.05). The results of immunofluorescence co-localization showed that the expressions of F4/80 and CD11c were low in the blank control group and the vehicle control group, while the expressions of F4/80 and CD11c were increased in the 2.5 mg·mL−1 and the 5.0 mg·mL−1 TCE groups. The results of immunohistochemistry showed that the expressions of CD16/32 and TNF-α in the blank control group and the vehicle control group were low, and there were large deposits in the 2.5 mg·mL−1 TCE group and the 5.0 mg·mL−1 TCE group. Conclusion The polarization of M1 KCs and the expression of proinflammatory factors may be related to an increased expression level of JMJD3 induced by oral TCE exposure.
