Invasion of dentinal tubules and pulp tissue by pathogenic bacteria may cause infection leading to pulpitis. Sirtuin 6 (SIRT6) is a NAD‐dependent protein deacetylase encoded by the SIRT6 gene. The effect of SIRT6 on lipopolysaccharide (LPS)‐induced pulpitis and its mechanism of action were discussed in this study. Dental pulp cells (DPCs) were extracted from human teeth and injected with LPS to induce inflammation. The cells injected with LPS showed substantially decreased expression of SIRT6. The overexpression of SIRT6, induced by plasmid‐transfection of DPCs with SIRT6 overexpressing vector, led to a marked decrease in proinflammatory cytokines (IL‐6, IL‐1β, and TNF‐α) and deactivation of NF kappa B pathway. Additionally, dentin matrix protein‐1 (DMP1), a promoter of inflammation in dental pulp tissues, was downregulated. Further investigation revealed that SIRT6 promotes ubiquitination of the transient receptor potential vanilloid 1 (TRPV1) channel, leading to its degradation and deactivation. The role of TRPV1 in the anti‐inflammatory effects of SIRT6 was determined through incubation of SIRT6‐expressing dental pulp stem cells (DPSCs) with capsaicin. This incubation counteracted the effect of SIRT6 on cytokines and DMP1. The injection of lentivirus‐SIRT6 attenuated LPS‐induced pulpitis in vivo by suppressing TRPV1 activity. Thus, SIRT6 inhibits the TRPV1 channel during LPS‐induced inflammation of dental pulp.

中文翻译：

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SIRT6的强大表达通过激活TRPV1通道抑制牙髓炎

病原菌侵入牙本质小管和牙髓组织可能导致感染，导致牙髓炎。Sirtuin 6（SIRT6）是由SIRT6基因编码的NAD依赖性蛋白脱乙酰酶。本研究讨论了SIRT6对脂多糖（LPS）引起的牙髓炎的作用及其作用机理。从人牙齿中提取牙髓细胞（DPC）并注射LPS以诱导炎症。注射LPS的细胞显示SIRT6的表达显着降低。SIRT6的过度表达是通过用过量表达SIRT6的载体对DPC进行质粒转染而引起的，导致促炎细胞因子（IL-6，IL-1β和TNF-α）的显着减少以及NFκB通路的失活。另外，牙髓组织炎症的启动子牙本质基质蛋白-1（DMP1）被下调。进一步的研究表明，SIRT6促进瞬态受体电位香草酸1（TRPV1）通道的泛素化，从而导致其降解和失活。通过将表达SIRT6的牙髓干细胞（DPSC）与辣椒素孵育，确定了TRPV1在SIRT6的抗炎作用中的作用。这种温育抵消了SIRT6对细胞因子和DMP1的作用。慢病毒SIRT6的注射通过抑制TRPV1的活性在体内减轻了LPS诱导的牙髓炎。因此，SIRT6在LPS诱导的牙髓炎症过程中抑制TRPV1通道。通过将表达SIRT6的牙髓干细胞（DPSC）与辣椒素孵育，确定了TRPV1在SIRT6的抗炎作用中的作用。这种温育抵消了SIRT6对细胞因子和DMP1的作用。慢病毒SIRT6的注射通过抑制TRPV1的活性在体内减轻了LPS诱导的牙髓炎。因此，SIRT6在LPS诱导的牙髓炎症过程中抑制TRPV1通道。通过将表达SIRT6的牙髓干细胞（DPSC）与辣椒素孵育，确定了TRPV1在SIRT6的抗炎作用中的作用。这种温育抵消了SIRT6对细胞因子和DMP1的作用。慢病毒SIRT6的注射通过抑制TRPV1的活性在体内减轻了LPS诱导的牙髓炎。因此，SIRT6在LPS诱导的牙髓炎症过程中抑制TRPV1通道。