Seul Ah Lee1, Bo-Ram Park2, Sung-Min Moon3, Sang Hun Shin1, Jae-Sung Kim4, Do Kyung Kim4, Chun Sung Kim5. 1. Department of Oral Biochemistry, College of Dentistry, Chosun University, 309 Pilmun-daero, Dong-gu, Gwangju, 61452, Republic of Korea. 2. Department of Dental Hygiene, College of Health and Welfare, Kyungwoon University, 730, Gangdong-ro, Gyeongsangbuk-do, 39160, Republic of Korea. 3. CStech Research Institute, 38 Chumdanventuresoro, Gwangju, 61007, Republic of Korea. 4. Oral Biology Research Institute, College of Dentistry, Chosun University, 309 Pilmun-daero, Dong-gu, Gwangju, 61452, Republic of Korea. 5. Department of Oral Biochemistry, College of Dentistry, Chosun University, 309 Pilmun-daero, Dong-gu, Gwangju, 61452, Republic of Korea. Electronic address: cskim2@chosun.ac.kr.
Abstract
OBJECTIVE: To investigate whether cynaroside protects human periodontal ligament (hPDL) cells from lipopolysaccharide (LPS)-induced damage and inflammation and to analyze the underlying mechanism. METHODS: LPS was used to stimulate hPDL and RAW264.7 cells. MTT assay was used to detect cell viability, and protein expression levels were measured via western blot analysis. Nitrite oxide and prostaglandin E2 were used to quantify the inflammatory response. Alizarin Red S staining was used to detect mineralized nodules. RESULTS: Cynaroside inhibited the expression of iNOS, COX-2, TNF-α, and IL-6 in LPS-stimulated hPDL and RAW264.7 cells without cytotoxicity. Furthermore, cynaroside significantly suppressed LPS-induced protein expression of matrix metalloproteinase 3. Additionally, cynaroside prevented LPS-induced NF-κB p65 subunit translocation to the nucleus by inhibiting the phosphorylation and degradation of IκB-α. Moreover, cynaroside could restore the mineralization ability of hPDL cells reduced by LPS. CONCLUSION: Cynaroside protected hPDL cells from LPS-induced damage and inflammation via inhibition of NF-κB activation. These results suggest that cynaroside may be a potential therapeutic agent for the alleviation of periodontitis.
OBJECTIVE: To investigate whether cynaroside protects human periodontal ligament (hPDL) cells from lipopolysaccharide (LPS)-induced damage and inflammation and to analyze the underlying mechanism. METHODS: LPS was used to stimulate hPDL and RAW264.7 cells. MTT assay was used to detect cell viability, and protein expression levels were measured via western blot analysis. Nitrite oxide and prostaglandin E2 were used to quantify the inflammatory response. Alizarin Red S staining was used to detect mineralized nodules. RESULTS:Cynaroside inhibited the expression of iNOS, COX-2, TNF-α, and IL-6 in LPS-stimulated hPDL and RAW264.7 cells without cytotoxicity. Furthermore, cynaroside significantly suppressed LPS-induced protein expression of matrix metalloproteinase 3. Additionally, cynaroside prevented LPS-induced NF-κB p65 subunit translocation to the nucleus by inhibiting the phosphorylation and degradation of IκB-α. Moreover, cynaroside could restore the mineralization ability of hPDL cells reduced by LPS. CONCLUSION:Cynaroside protected hPDL cells from LPS-induced damage and inflammation via inhibition of NF-κB activation. These results suggest that cynaroside may be a potential therapeutic agent for the alleviation of periodontitis.