N-acetylcysteine prevents LPS-induced pro-inflammatory cytokines and MMP2 production in gingival fibroblasts
N-acetylcysteine prevents LPS-induced pro-inflammatory cytokines and MMP2 production in gingival fibroblasts
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DOI：
10.1007/bf02980269
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发表时间：
2007-10-01
影响因子：
6.7
通讯作者：
Han, Soo-Boo
中科院分区：
文献类型：
--
作者：
Kim, Do Young;Jun, Ji-Hae;Han, Soo-Boo
牙周炎是一种炎症过程，最终导致牙齿脱落。虽然牙周炎的主要病原体是细菌，但大多数牙周组织破坏被认为是由不适当的宿主反应引起的。活性氧（ROS）参与牙周组织的破坏。我们用从大肠杆菌中获得的脂多糖（LIPS）处理人牙龈成纤维细胞。大肠杆菌和牙周病原体放线杆菌放线菌和牙龈卟啉单胞菌，并检查其炎症反应的存在和不存在的抗氧化剂N-乙酰半胱氨酸（NAC）。LPS增强ROS的产生，以及促炎细胞因子如白细胞介素-10、白细胞介素-6、白细胞介素-8和肿瘤坏死因子-α的表达，以及MMP 2的产生和活化。NAC抑制了所有LPS诱导的炎症反应，这表明LPS诱导的ROS可能在牙龈成纤维细胞的这些反应中发挥重要的调节作用。此外，NAC阻止LPS诱导的p38 MAPK和JNK的活化，但不阻止IkB的磷酸化和随后的降解。这些结果表明，NAC在LPS刺激的牙龈成纤维细胞中发挥抗炎作用，至少部分地通过下调JNK和p38 MAPK活化发挥作用。此外，这项工作表明，抗氧化剂可能是有用的，补充传统的牙周治疗的预防性治疗。
Periodontitis is an inflammatory process that ultimately results in tooth loss. Although the primary etiologic agent for periodontitis is bacteria, the majority of periodontal tissue destruction is thought to be caused by an inappropriate host response. Reactive oxygen species (ROS) have been known to be involved in periodontal tissue destruction. We treated human gingival fibroblasts with lipopolysaccharide (LIPS) obtained from E. coli and the periodontopathogens Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis, and examined their inflammatory responses in the presence and absence of the antioxidant N-acetylcysteine (NAC). LPS enhanced ROS production, as well as, expression of pro-inflammatory cytokines such as interleukin-1 0, interleukin-6, interleukin-8 and tumor necrosis factor-(x, and the production and activation of MMP2. NAC suppressed all LPS-induced inflammatory responses examined, suggesting that LPS-induced ROS may play a major regulatory role in these responses in gingival fibroblasts. In addition, NAC prevented LPS-induced activation of p38 MAPK and JNK but not phosphorylation and subsequent degradation of IkB. These results indicate that NAC exerts anti-inflammatory effects in LPS-stimulated gingival fibroblasts, functioning at least in part via down-regulation of JNK and p38 MAPK activation. Furthermore, this work suggests that antioxidants may be useful in adjunctive therapies that complement conventional periodontal treatments.