1.In vitro biomimetic remineralization of dentin collagen by phosphorylated chitosan/amorphous calcium phosphate compound and tripolyphosphate
Ruijing MIAO ; Xu ZHANG ; Yingchun SUN ; Ping GAO
Tianjin Medical Journal 2015;43(5):518-521,579
Objective To investigate the remineralizing therapy of deep caries and in vitro biomimetic remineralization of demineralized dentin by phosphorylated chitosan/amorphous calcium phosphate compound (P-chi/ACP) and tripolyphosphate (TPP). Methods Thirty-two extracted human molars were cut and completely demineralized. Two samples were used to show the characteristics by transmission electron microscopy (TEM). The other 30 samples were divided into two groups:fifteen samples were treated by P-chi/ACP and TPP (P-chi/ACP+TPP group), the other fifteen samples were not treated by TPP (P-chi/ACP group). All of the samples were distinguished into experimental side and control side, and then they were set on the in vitro model for 1 week. Micro-computed tomography (μCT) and TEM were used to assess the effects of remineralization. Results μCT detection revealed that the mineral density were higher in the experimental sides (125.42±12.16 and 119.39±8.64) than that of control sides (96.96±10.56 and 105.27±9.42) in both groups (P<0.01). TEM figures showed that hierarchical intrafibrillar remineralization was realized in samples of P-chi/ACP+TPP group, while trace amounts of hierarchical remineralization was detected in P-chi/ACP group. Conclusion Fully demineralized dentin appears to have the potential to be remineralized with the application of P-chi/ACP. The ultrastructure of samples is better in P-chi/ACP+TPP group than that of P-chi/ACP group.
2.Modified Shengjiangsan Inhibits Necroptosis by Mediating RIP1/RIP3/MLKL Signaling Pathway and Reduces Renal Fibrosis in Rats with Diabetic Nephropathy
Ruijing SONG ; Xinxin ZHANG ; Fei GAO ; Miao TAN ; Jinchuan TAN
Chinese Journal of Experimental Traditional Medical Formulae 2022;28(17):33-42
ObjectiveTo observe the mechanism of modified Shengjiangsan in necroptosis and renal fibrosis of rats with diabetic nephropathy based on receptor-interacting protein (RIP)1/RIP3/mixed lineage kinase domain-like protein (MLKL) signaling pathway. MethodSeventy-five SD rats were randomly divided into a model group, a normal group, three high, medium, and low-dose modified Shengjiangsan groups (4.365, 8.73, 17.46 g·kg-1), and an irbesartan group (0.013 5 g·kg-1). After 4 weeks of intragastric administration, the levels of 24 h urine protein (UTP), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) of rats in each group were determined, as well as the changes in degree of renal pathology. Real-time quantitative polymerase chain reaction (Real-time PCR) and immunohistochemistry were used to detect the mRNA and protein expression levels of IL-1β, TNF-α, monocyte chemoattractant protein-1 (MCP-1), transforming growth factor-β1 (TGF-β1), and nuclear factor kappa B (NF-κB) in kidney tissues of rats. Western blot assay was used to detect the expression levels of key proteins in the RIP1/RIP3/MLKL signaling pathway. ResultAs compared with the normal group, the renal interstitial fibrosis in the model group was obvious, and the 24 h UTP, IL-1β, TNF-α levels were significantly increased (P<0.05). In the model group, the mRNA and protein expression levels of IL-1β, TNF-α, MCP -1, TGF-β1, and NF-κB in the kidney tissues were significantly increased (P<0.05), and protein expression levels of RIP1, RIP3, p-MLKL, and MLKL were significantly increased (P<0.05). Compared with the model group, all modified Shengjiangsan groups and the irbesartan group improved the levels of renal interstitial fibrosis in rats to varying degrees. As compared with the model group, the 24 h UTP levels in all modified Shengjiangsan groups and the irbesartan group were decreased to varying degrees (P<0.05), the content of IL-1β and TNF-α in the serum were decreased (P<0.05), the mRNA and protein expression levels of IL-1β, TNF-α, MCP-1, TGF-β1, and NF-κB in renal tissues was down-regulated (P<0.05), and the protein expression levels of RIP1, RIP3, p-MLKL, and MLKL were down-regulated (P<0.05). ConclusionModified Shengjiangsan ameliorates renal injury of rats with diabetic nephropathy, and the mechanism may be related to the down-regulation of the RIP1/RIP3/MLKL signaling pathway, the prevention of renal tissue necroptosis, and the inhibition of renal fibrosis.