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1.
Journal of Peking University(Health Sciences) ; (6): 24-29, 2020.
Article in Chinese | WPRIM | ID: wpr-941961

ABSTRACT

OBJECTIVE@#To study the effects of non-steroidal anti-inflammatory drugs (NSAIDs) on anti-inflammation and repair of human dental pulp cells (hDPCs).@*METHODS@#Primary hDPCs from the freshly extracted human third molars were cultured and passaged in vitro, and the following experiments were performed using the 4th-6th generations of hDPCs. HDPCs were cultured in Dulbecco's modified eagle medium (DMEM) containing 1 mg/L lipopolysaccharide (LPS) to obtain LPS irritated hDPCs (LPS-hDPCs), which served as the inflammatory positive group. LPS-hDPCs in the experimental group were cultured in DMEM containing different concentrations (1, 10, and 100 μmol/L) of NSAIDs (aspirin or meloxicam). HDPCs cultured in DMEM were used as the negative control group. The effects of NSAIDs on the proliferation of hDPCs were assessed on the 1st, 3rd, 5th, and 7th day by MTT assay. The effects of NSAIDs on the expression of inflammation related genes interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) of LPS-hDPCs were detected at the 6th hour by real-time PCR. The expression of differentiation related markers dentin matrix protein-1 (DMP-1) and dentin sialophosphoprotein (DSPP) were detected on the 7th day by real-time PCR. The effects of NSAIDs on the mineralization of LPS-hDPCs were assesd on the 14th day by alizarin red staining. Calcium mineralized nodules were semi-quantitatively determined by cetyl pyridine chloride.@*RESULTS@#MTT assay showed that 1-100 μmol/L aspirin or meloxicam significantly promoted the proliferation of hDPC in a concentration dependent manner (P<0.05). Real-time PCR showed that 1-100 μmol/L meloxicam or 100 μmol/L aspirin down-regulated significantly the mRNA expression of TNF-α and IL-6 of LPS-hDPCs (P<0.05), and 100 μmol/L meloxicam down-regulated IL-6 and TNF-α more significantly than 100 μmol/L aspirin of LPS-hDPCs (P<0.05). Real-time PCR showed that 100 μmol/L meloxicam up-regulated the mRNA expression of DMP-1 and DSPP of LPS-hDPCs significantly (P<0.05). Alizarin red staining showed the meloxicam at the concentration of 100 μmol/L significantly promoted the mineralization of LPS-hDPCs (P<0.05).@*CONCLUSION@#In this study, meloxicam promoted the proliferation of hDPCs, inhibited the inflammatory reaction and promoted differentiation and mineralization of hDPCs under LPS irritation. The present results suggest that meloxicam may play a role in anti-inflammation and repair of pulp inflammation.


Subject(s)
Humans , Anti-Inflammatory Agents, Non-Steroidal , Cell Differentiation , Cell Proliferation , Cells, Cultured , Dental Pulp
2.
Chinese Journal of Immunology ; (12): 765-768,773, 2018.
Article in Chinese | WPRIM | ID: wpr-702814

ABSTRACT

The inflammasome is a kind of multi-protein complexes with high molecular weight that can induce cells to die under the pathological conditions of inflammation and stress.After spinal cord injury,there are a variety of immune cells with different functions in the local injured microenvironment.Under natural conditions,the immune cell subsets in the local injured microenvironment are imbalance in"yin and yang",and the destructive subpopulations and cytokines are dominant.This is an important mechanism of pathological damage caused by SCI.Inflammasome plays an extremely important role in the process of central nervous system injury.Although activation of inflammasome and IL-1β and IL-18 are all expressed at the site of injured spinal cords,their effects on local immune microenvironment of SCI have not yet been reported.According to the current research progress,we believe that activation of inflammasome can affect the local immune microenvironment of SCI.This is an interesting topic,but few related studies have been re-ported.This review focuses on four types of inflammasomes associated with CNS injury.Their structure,function and so on will be ex-pounded.The relationship between inflammasome activation and immune microenvironment of SCI will also be discussed.

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