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三七正丁醇提取物通过抑制 LPS 激活的 RAW264.7 细胞中的 MAPK 抑制牙周膜成纤维细胞中 LPS 诱导的 MMP-2 表达并抑制破骨细胞生成。

n-Butanol extracts of Panax notoginseng suppress LPS-induced MMP-2 expression in periodontal ligament fibroblasts and inhibit osteoclastogenesis by suppressing MAPK in LPS-activated RAW264.7 cells.

机构信息

WCU Department of Nanobiomedical Sciences, Dankook University, Republic of Korea.

出版信息

Arch Oral Biol. 2011 Nov;56(11):1319-27. doi: 10.1016/j.archoralbio.2011.05.010. Epub 2011 Jun 23.

DOI:10.1016/j.archoralbio.2011.05.010
PMID:21703595
Abstract

OBJECTIVE

Periodontitis is a group of inflammatory diseases that affect connective tissue attachments and the supporting bone that surround the teeth. Osteoclasts are responsible for skeletal modeling and remodeling but may also destroy bone in several bone diseases, including osteoporosis and periodontitis. This study examined the anti-inflammatory effects of Panax notoginseng (PN) on periodontal ligament fibroblasts (PDLFs) and RAW264.7 cells under lipopolysaccharide (LPS) induced inflammatory conditions.

DESIGN

The effects of PN on PDLFs were determined by measuring the cell viability and mRNA expression of tissue-destructive proteins. The effects of PN on osteoclasts were examined by measuring the following: (1) the cell viability, (2) the formation of Tartrate-resistant acid phosphatase (TRAP)(+) multinucleated cells, (3) MAPK signaling pathways, (4) mRNA expression of inflammatory-related proteins and (5) nitric oxide (NO) production.

RESULTS

The n-butanol extracts of PN (bPN) increased the cell proliferation of the PDLFs and decreased the mRNA expression of matrix metalloproteinase (MMP)-2 in the PDLFs. bPN inhibited the formation of LPS-stimulated TRAP(+) multinucleated cells. bPN also inhibited the LPS-stimulated activation of JNK and ERK signaling, and inhibited the LPS-stimulated degradation of I(K)B in the RAW264.7 cells. In addition, bPN decreased the mRNA expression of MMP-9 and iNOS, which are involved in the range of pathophysiological processes, such as inflammation in the RAW264.7 cells. NO production was also decreased via the inhibition of iNOS.

CONCLUSIONS

These findings suggest that bPN has therapeutic effects on bone-destructive processes, such as those that occur in periodontal diseases.

摘要

目的

牙周炎是一组影响牙齿周围结缔组织附着和支持骨的炎症性疾病。破骨细胞负责骨骼的塑造和重塑,但也可能破坏几种骨骼疾病中的骨,包括骨质疏松症和牙周炎。本研究探讨了三七(PN)在脂多糖(LPS)诱导的炎症条件下对牙周膜成纤维细胞(PDLFs)和 RAW264.7 细胞的抗炎作用。

设计

通过测量组织破坏性蛋白的 mRNA 表达和细胞活力来确定 PN 对 PDLFs 的影响。通过测量以下指标来研究 PN 对破骨细胞的影响:(1)细胞活力,(2)抗酒石酸酸性磷酸酶(TRAP)(+)多核细胞的形成,(3)MAPK 信号通路,(4)炎性相关蛋白的 mRNA 表达和(5)一氧化氮(NO)的产生。

结果

PN 的正丁醇提取物(bPN)增加了 PDLFs 的细胞增殖,并降低了 PDLFs 中基质金属蛋白酶(MMP)-2 的 mRNA 表达。bPN 抑制了 LPS 刺激的 TRAP(+)多核细胞的形成。bPN 还抑制了 LPS 刺激的 JNK 和 ERK 信号通路的激活,并抑制了 LPS 刺激的 RAW264.7 细胞中 I(K)B 的降解。此外,bPN 降低了 MMP-9 和 iNOS 的 mRNA 表达,这与炎症等一系列病理生理过程有关。通过抑制 iNOS,NO 的产生也减少了。

结论

这些发现表明,bPN 对骨破坏性过程具有治疗作用,例如牙周病中发生的过程。

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