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BACKGROUND: Previous studies have shown that puerarin can inhibit the differentiation of osteoclasts, and the expression of Notch signaling pathway-related proteins such as Notch1, HES1, and Jagged1 is decreased. However, the specific mechanism of the Notch1 signaling pathway for the inhibition of osteoclast differentiation by puerarin is not clear. OBJECTIVE: To explore the effect of Notch signaling pathway on puerarin inhibiting the differentiation of mouse macrophage Raw264.7 into osteoclasts. METHODS: Raw264.7 cells were divided into seven groups for intervention culture. Blank control group was cultured in high-sugar DMEM medium; the osteoclast induction group was cultured in osteoclast induction medium; the puerarin intervention group was cultured with 50 μmol/L puerarin at the same time of osteoclast induction; Notch1 siRNA control group, Notch1 siRNA group, Notch1 overexpression control group and Notch1 overexpression group were transfected with Notch1 siRNA control sequence, Notch1 siRNA, Notch1 overexpression control plasmid and Notch1 overexpression plasmid, respectively, and then cultured with osteoclast induction medium and puerarin. The number and size of osteoclasts were observed by tartrate-resistant acid phosphatase staining, the skeleton formation of osteoclasts was observed by F-actin staining, and the gene expression level of osteoclast formation markers was detected by RT-PCR. RESULTS AND CONCLUSION: Tartrate-resistant acid phosphatase staining results showed that puerarin intervention could inhibit the generation of osteoclasts, Notch1 silencing could further reduce the number of osteoclasts, while the number of osteoclasts in the osteoclast-induced group increased significantly after Notch1 overexpression. The results of F-actin showed that Raw264.7 cells could form a well-defined F-actin ring after osteoclast induction. Puerarin intervention would inhibit the formation of cytoskeleton, and Notch1 silencing could aggravate the inhibitory effect of cytoskeleton formation, while Notch1 overexpression could alleviate this inhibitory effect of puerarin. RT-PCR results showed that puerarin could inhibit the mRNA expression levels of tartrateresistant acid phosphatase, Cathepsin K and c-Fos, the expression of the above-mentioned three factors decreased significantly after Notch1 gene silencing, and Notch1 overexpression could upregulate the expression of these factors. These finding indicate that puerarin inhibits the differentiation of Raw264.7 cells into osteoclasts through the Notch signaling pathway. [ABSTRACT FROM AUTHOR]

BACKGROUND: In recent years, numerous studies have shown that long non-coding RNAs (lncRNAs) have an important role in the pathogenesis of periodontitis, including the immune response process and the biological activity and function of cells (periodontal stem cells and osteoblasts). Researchers attempt to regulate periodontal inflammation and periodontal regeneration by regulating lncRNA expression levels. OBJECTIVE: To review the progress of research on lncRNAs in periodontitis, thereby advancing the research of lncRNAs in periodontitis. METHODS: The first author searched PubMed, China National Knowledge Infrastructure (CNKI), Web of Science database, and WanFang Database for relevant literature published up to March 2023. “Long non-coding RNA, lncRNA, periodontitis, periodontium, immunity, inflammation, periodontal ligament stem cells, osteoclasts, osteogenic differentiation, bone resorption, bone formation, recurrence, hypoxia, oxidative stress, static mechanical strain”were used as the Chinese search terms. “lncRNA, periodontitis, periodontal, immunity, inflammation, periodontal membrane stem cells, osteoclasts, osteogenic differentiation, bone resorption, bone formation, recurrence, hypoxia, oxidative stress, static mechanical strain” were used as the English search terms. The title and abstract of each paper were read for initial screening, and 87 papers were finally selected for inductive analysis. RESULTS AND CONCLUSION: Periodontal pathogens stimulate the body, leading to immune imbalance that triggers inflammatory response and destroy periodontal tissue, and lncRNAs are involved in its regulatory mechanism. LncRNAs are involved in the pro-inflammatory regulation of periodontal ligament cells in an inflammatory environment, and their effects on osteoclast differentiation are regulated through ceRNA mechanism, which provides new clues for exploring the pathogenesis of periodontitis. For B cells and macrophages, lncRNAs can regulate the infiltration, cell activity and function of their subsets in periodontitis. LncRNAs participate in the immune response related to periodontitis mainly through two pattern recognition receptors, Toll-like receptors and NOD-like receptors, and nuclear factor-κB signaling pathway. To investigate whether lncRNAs can be used as a biomarker of periodontitis has great value in the diagnosis and prognosis of periodontitis. Animal experiments have demonstrated that the role of lncRNAs in periodontitis can be reversed by modulating the expression level of lncRNAs and thus lncRNAs act as an anti-inflammatory agent, which is of great value for the study of immunotherapy in periodontitis. The regulation of lncRNAs on periodontal ligament stem cells is mainly realized through endogenous competition mechanism and various signaling pathways, and its effects are influenced by various factors, such as inflammatory environment, mechanical strain, hypoxia and oxidative stress. Research on related mechanisms through these related factors provides new ideas for the treatment of periodontitis. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: In recent years, many studies have confirmed that assembloids can make up for the shortcomings of organoids, which cannot fully reproduce the interaction between cell and cell and between cell and matrix. Since the assembloids construction methods are in the early stage of development, there is no unified standard. OBJECTIVE: To review the current construction methods, applications, advantages, and disadvantages of assembloids, guide the development and improvement of vitro cell models. METHODS: PubMed, CNKI, and WanFang databases were searched with English search terms “assembloids, organoids, tumor microenvironment, organoids AND assemble, organoids AND microenvironment” and Chinese search terms “assembloids, organoids, tumor microenvironment, organoid reorganization, multicellular model”. Totally 94 articles were screened out for review after excluding irrelevant articles and deduplication. RESULTS AND CONCLUSION: (1) According to the different sources of cells, the construction of assembloids can be divided into three methods: self-assembly, direct-assembly, and mixed-assembly. According to the differences of cell culture methods, it can be divided into suspension culture method, matrix culture method, organ chip culture method, and 3D bio-printing. (2) The process of self-assembly covers early stages of cell and tissue development, so it has broad prospects in the fields of organ development and developmental disorders. The function of differentiated mature cells is relatively perfect, and the assembloids directly assembled by them have more potential in the study of functional disorders and cell-damaging diseases. Self-assembly may be better in organ transplantation, and direct-assembly will be more suitable for the repair of tissue damage. Mixed-assembly combines the advantages of the former two and is mostly used to explore the physiological and pathological mechanisms of cells in the microenvironment, as well as drug screening. (3) Although different assembloids have their own advantages, they all face the problem of imperfect vasculature system, then, each method has its own limitations, for example, the degree of cell differentiation in self-assembly assembloids may still be different from that in vivo, and the fixed cell types in direct-assembly models cannot simulate complex microenvironments in vivo. These are urgent problems to be solved. (4) In the future, with the continuous improvement of assembloids culture technology, scientists can assemble biomimetic organoids with more complex tissues in vitro, providing infinitely realistic models for the study of physiological and pathological processes of human tissue and organ. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Puerarin is a flavonoid derivative from Pueraria lobata. Studies have found that puerarin can prevent osteoporosis and promote new bone formation, which is expected to become a potential drug for treating diseases related to bone destruction. OBJECTIVE: To observe the effect of puerarin on osteoclast differentiation of RAW264.7 cells and to explore the regulatory effect of Notch signaling pathway. METHODS: RAW264.7 cells were divided into five groups: control group treated with Dulbecco’s modified Eagle medium high sugar medium; osteoclast induction group treated with osteoclast induction medium (Dulbecco’s modified Eagle medium high sugar medium containing macrophage colony-stimulating factor and receptor activator of nuclear factor-κB ligand); low-, medium- and high-concentration puerarin groups treated with osteoclast induction medium containing 10, 25 and 50 μmol/L puerarin respectively. After 7 days of culture, tartrate-resistant acid phosphatase staining and F-actin staining were used to observe the role of puerarin in osteoclast formation. RT-PCR was used to detect the expression of genes related to osteoclast formation. Western blot and RTPCR were used to detect the expression of Notch signaling pathway-related indicators. RESULTS AND CONCLUSION: Tartrate-resistant acid phosphatase staining results indicated that osteoclast formation ability was enhanced in the osteoclast induction group compared with the control group (P < 0.01), while compared with the osteoclast induction group, low-, middle-, and high-concentration puerarin intervention inhibited osteoclast formation in a concentration-dependent manner (P < 0.05, P < 0.01). F-actin staining results revealed that clear ring structure could be observed in the osteoclast induction group; compared with the osteoclast induction group, puerarin intervention could inhibit the formation of F-actin ring in a concentration-dependent manner. RT-PCR results showed that compared with the control group, the expression of tartrateresistant acid phosphatase, cathepsin K and C-fos mRNA was increased in the osteoclast induction group (P < 0.01); compared with the osteoclast induction group, puerarin intervention decrease the expression of tartrate-resistant acid phosphatase, cathepsin K and C-fos mRNA in a concentration-dependent manner (P < 0.01). Western blot and RT-PCR results showed that the expression of Notch1, Notch2, Hes1, Jagged1 and Jagged2 was increased in the osteoclast induction group compared with the control group (P < 0.01); compared with the osteoclast induction group, puerarin intervention reduced the expression of Notch1, Notch2, Hes1, Jagged1, and Jagged2 in a concentration-dependent manner (P < 0.01). To conclude, puerarin inhibits the osteoclast differentiation ability of RAW264.7 cells by inhibiting the Notch signaling pathway. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Periodontitis is an inflammation of the periodontal support tissue, manifested as inflammation of the gums and resorption of alveolar bone. Macrophages can play a role in the occurrence and development of periodontitis through M1 and M2 polarization. OBJECTIVE: To review the relationship between macrophage polarization and periodontitis and its related mechanism, so as to provide ideas for the clinical treatment of periodontitis. METHODS: The first author searched the relevant papers published from 1991 to 2022 in PubMed and CNKI. The search terms in Chinese and English were “macrophage polarization, M1/M2 macrophages, periodontitis.” Preliminary screening was performed by reading the title and abstract. Finally, 97 articles were included and analyzed. RESULTS AND CONCLUSION: As human innate immune cells, macrophages play an important role in the occurrence and development of inflammation. Macrophages can be polarized under environmental stimulation, which is a complex process. Signaling pathways such as JAK/STAT, TLRs/nuclear factor-κB, PI3K/ Akt, inflammatory factors such as tumor necrosis factor-α, interferon-γ, interleukin-4, interleukin-13, and epigenetic mechanisms can all influence macrophage polarization. M1-type polarization of macrophages promotes inflammatory progression and M2-type polarization of macrophages exerts anti-inflammatory effects. Studies have found that different polarized types of macrophages play a pro-inflammatory or anti-inflammatory role in the process of periodontitis through various signaling pathways and secretion of inflammatory factors, and influence bone resorption and bone formation through a variety of ways, and then affect the progression of periodontitis. That is, macrophages are polarized through relevant mechanisms and the polarized macrophages can play an anti-inflammatory or pro-inflammatory role in the process of periodontitis, which has an impact on the progression of periodontitis. Therefore, it is of great significance for the treatment of periodontitis to study the role and mechanism of macrophage polarization in the pathogenesis of periodontitis. However, the polarization mechanism of macrophages is not completely clear yet. Therefore, it is of great significance for future treatment of periodontitis to discover the potential mechanism of polarization and combine it with the treatment of periodontitis to promote the transformation of macrophages to M2-type and its proportion or inhibit or reduce the expression of M1-type macrophages in the process of periodontitis. The combination of epigenetics with macrophage polarization and periodontitis at the gene and protein levels may be an effective treatment for periodontitis. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Strontium promotes bone formation, and reduces bone resorption. Strontium-modified titanium implant surface has been the focus of research in implant osseointegration under osteoporotic conditions. OBJECTIVE: To investigate the cell adhesion, stretch, and migration of advanced strontium-modified titanium surfaces using bone marrow mesenchymal stem cells isolated from rats. METHODS: Strontium-modified titanium surfaces were produced by sequential treatments with 5 mol/L NaOH, 100 mmol/L strontium acetate, and heated at 600 or 700 °C for 1 hour. After heat treatment, half the samples were soaked in deionized water at 80 °C for 24 hours, then washed and dried. The pure titanium served as control group, and there were five groups. The whole bone marrow adherence method was used to separate bone marrow mesenchymal stem cells from the rats. The modified titanium sheets were placed in 24-well plates and cultured in cell suspension. Cell adhesion and cell proliferation were assessed using cell counting kit-8 assay. After bone marrow mesenchymal stem cells were with the titanium sheet for 24 hours, the actin was stained to observe cell adhesion and stretch. The migration of bone marrow mesenchymal stem cells on different titanium surfaces was investigated using cell scratch test and fluorescence staining. The expression levels of collagen type І, Runx2, osteoprotegerin, RANKL and osteopontin were detected by qRT-PCR. RESULTS AND CONCLUSION: Strontium-modified titanium could promote the stretch and migration of bone marrow mesenchymal stem cells. The number of proliferative cells in the Sr700 group was significantly higher than that in the Sr600 group at 5 days (P < 0.01). On day 14, strontium-modified titanium promoted the expression of collagen type І, Runx2, and osteopontin. In summary, strontium-modified titanium can promote adhesion, spreading, migration and proliferation of rat bone marrow mesenchymal stem cells. Moreover, hydration treatment can enhance the osteogenic activity of rat bone marrow mesenchymal stem cells. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)