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»ç¶÷ Ä¡ÁÖÀδ뼼Æ÷¿¡¼­ Lipopolysaccharide¿Í ´ÏÄÚƾÀ¸·Î À¯µµµÈ iNOS¿Í COX-2 ¹ßÇö¿¡ NFATcÀÇ °ü¿©

NFATc Mediates Lipopolysaccharide and Nicotine-Induced Expression of iNOS and COX-2 in Human Periodontal Ligament Cells

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ÀÌ»óÀÓ ( Lee Sang-Im ) - ´Ü±¹´ëÇб³ º¸°Ç°úÇдëÇÐ Ä¡À§»ýÇаú
À¯Áö¼ö ( Yu Ji-Su ) - ±¸¹Ì´ëÇб³ Ä¡À§»ý°ú

Abstract

¼÷ÁÖ ¸é¿ª ¹ÝÀÀ°ú ¸é¿ª ü°è´Â Ä¡ÁÖ Áúȯ¿¡ ´ëÇÑ °³ÀÎÀÇ°¨¼ö¼ºÀÇ ÁÖ¿ä ¿øÀÎÀÌ´Ù. ¼¼±Õ °¨¿°°ú Èí¿¬Àº Ä¡ÁÖ Á¶Á÷ÀÇÆı«ÀÇ ¿øÀΰú ÁøÇà¿¡ °ü¿©ÇÏ´Â Áß¿äÇÑ È¯°æ À§Çè ¿äÀÎÀÌ´Ù. µû¶ó¼­, º» ¿¬±¸´Â »ç¶÷ Ä¡ÁÖÀδ뼼Æ÷¿¡¼­ LPS¿Í ´ÏÄÚƾÀÌ Àü¿°Áõ¼º »çÀÌÅäÄ«ÀÎÀÎ iNOS/COX-2ÀÇ ¹ßÇö°ú NO/ PGE2 »ý»ê¿¡ ¹ÌÄ¡´Â ¿µÇâÀ» ¾Ë¾Æº¸°í NFATc1°¡ ¾î¶² ±âÀüÀ¸·Î Ç׿°ÀÛ¿ëÀ» ÇÏ´ÂÁö ¹àÈ÷°íÀÚ ÇÏ¿´´Ù. LPS¿Í ´ÏÄÚƾÀ» ó¸®ÇÑ »ç¶÷ Ä¡ÁÖÀδ뼼Æ÷¿¡¼­ iNOS/COX-2ÀÇ ¹ßÇö°úÇÔ²² NO/PGE2 »ý»êÀº Áõ°¡µÇ¾ú´Ù. NFATc1 inhibitorÀÎCsA´Â LPS¿Í ´ÏÄÚƾ¿¡ ÀÇÇØ À¯µµµÇ´Â iNOS/COX-2ÀÇ ¹ßÇö°ú ÇÔ²² NO/PGE2 »ý»êÀ» °¨¼Ò½ÃÄ×´Ù. ÀÌ·¯ÇÑ ¿¬±¸ °á°ú·Î º¼ ¶§, NFAT signaling pathway°¡ LPS¿Í ´ÏÄÚƾ¿¡ ÀÇÇÑiNOS/COX-2ÀÇ ¹ßÇöÀ» Á¶ÀýÇÏ¿© NO/PGE2 ¸Å°³ ¿°Áõ¿¡´ëÇØ ¹æ¾îÇÒ ¼ö ÀÖ´Ù°í »ý°¢µÈ´Ù.

Although nuclear factor of activated T cell (NFAT) plays a key role in inflammation, its anti-inflammatory effects and mechanism of action in periodontitis are still unknown. This study aimed to identify the effects of NFAT on the proinflammatory mediators activated by lipopolysaccharide (LPS) plus nicotine stimulation in human periodontal ligament cells (hPDLCs). The production of nitric oxide (NO) and prostaglandin E2 (PGE2) was evaluated using Griess reagent and an enzyme immunoassay, respectively. The expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and NFAT proteins was evaluated by Western blot analysis. LPS plus nicotine synergistically induced the production of NO and PGE2 and increased the protein expression of iNOS, COX-2 and NFAT. Treatment with an NFAT inhibitor blocked the LPS plus nicotine-stimulated NO and PGE2 release as well as the expression of iNOS and COX-2. Our data suggest that the LPS plus nicotine-induced inflammatory effects on hPDLCs may act through a novel mechanism involving the action of NFAT. Thus, NFAT may provide a potential therapeutic target for the treatment of periodontal disease associated with smoking and dental plaque.

Å°¿öµå

Lipopolysaccharides; NFATc transcription factors; Nicotine; Periodontitis

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