1.Impacts of soy isoflavones inhibiting Slit2/MAPK signaling pathway on alveolar bone resorption and inflammatory response in periodontitis rats
Zheying DAI ; Yi GUO ; Yang LIU ; Wenjia LI ; Hui ZHOU
Chinese Journal of Immunology 2024;40(6):1131-1136
Objective:To investigate impacts of soy isoflavones(SIF)on alveolar bone resorption and inflammatory response in periodontitis rats based on Slit homologue 2(Slit2)/P38 mitogen-activated protein kinase(MAPK)signaling pathway.Methods:Rats were separated into Control group,Model group,SIF low-dose group(L-SIF,25 mg/kg)and SIF high-dose group(H-SIF,75 mg/kg),with 10 rats per group,and periodontitis model was established by ligating necks of maxillary first molars of rats with silk thread except for control group.Rats in L-SIF group and H-SIF group were given corresponding doses of SIF by gavage,Control group and Model group were given same amount of normal saline by gavage,once a day,for 4 consecutive weeks.After administration,serum Slit2,TNF-α,IL-6 and IL-1β levels were detected by ELISA;Micro-CT scan was performed to detect distance between cemen-tumenamel junction and alveolar ridge crest(CEJ-ABC),bone mineral density(BMD),bone volume fraction(BV/TV),and alveolar bone loss was evaluated;HE staining and tartrate-resistant acid phosphatase(TRAP)staining were performed to evaluate tissue inflam-mation,bone resorption and osteoclast activity;expressions of osteoprotegerin(OPG)and receptor activator of nuclear factor κB ligand(RANKL)in periodontal tissues were detected by immunohistochemistry(IHC);Western blot was performed to detect protein expressions of Slit2,P38 MAPK and p-P38 MAPK in periodontal tissues.Results:Compared with Control group,serum levels of Slit2,TNF-α,IL-1β,IL-6,CEJ-ABC distance,periodontal histopathological damage score,osteoclast number,positive expression of RANKL,protein level of Slit2 and p-P38 MAPK/P38 MAPK were greatly increased in Model group,BMD,BV/TV and positive ex-pression of periodontal tissues OPG were greatly decreased(all P<0.05);compared with Model group,serum levels of Slit2,TNF-α,IL-1β,IL-6,CEJ-ABC distance,periodontal histopathological damage score,osteoclast number,positive expression of RANKL,pro-tein levels of Slit2 and p-P38 MAPK/P38 MAPK were greatly decreased,BMD,BV/TV and OPG positive expression of periodontal tissues were greatly increased in L-SIF group and H-SIF group(P<0.05),the above indicators in H-SIF group changed greatly better than L-SIF group(P<0.05).Conclusion:SIF can inhibit alveolar bone resorption and inflammatory response in periodontitis rats and improve periodontitis,whose mechanism may be related to inhibition of Slit2/P38 MAPK signaling pathway.
2.The effects of circulating exosomes derived from oral cancer patients on the proliferation, migration and invasiveness of tongue cancer CAL27 cells
Yi GUO ; Hong PENG ; Shujuan JIAN ; Hui CHEN ; Zheying DAI ; Ling JIANG ; Xiuchen LI ; Xiaoyan CUI
Journal of Practical Stomatology 2019;35(1):60-65
Objective: To investigate the effects of circulating exosomes derived from oral cancer patients on the proliferation, migration and invasion of tongue cancer CAL27 cells. Methods: Circulating exosomes were isolated from the peripheral blood of 20 oral cancer patients using gradient centrifugation. The characteristics of the exosome was studied by transmission electron microscope (TEM) and Western blot. After treatment with circulating exosomes, CAL27 cell proliferation was evaluated with MTT assay, migration was observed by cell wound scratch assay and the invasion of CAL27 cells was tested by Transwell assay. CAL27 cell bearing nude mice were used to estimate the effect of circulating exosome on CAL27 cell proliferation and metastasis in vivo. Results: The proliferation, migration and invasion of CAL27 cells were enhanced by circulating exosomes from oral cancer patients. In vivo study showed that the tumorigenesis and metastasis of CAL27 cells were enhanced by circulating exosomes. Conclusion: Circulating exosomes from oral cancer patients can promote the proliferation, migration, invasion and metastasis of CAL27 cells.