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Mahmoud Hashemi, Ali, Solahaye Kahnamouii, Shiva, Aghajani, Hassan, Frozannia, Khalil, Pournasrollah, Alireza, Sadegh, Rasoul, Esmaeeli, Heidarali, Ghadimi, Yosef, Razmpa, Ebrahim. (1397). Quercetin Decreases Th17 Production by Down-Regulation of MAPK- TLR4 Signaling Pathway on T Cells in Dental Pulpitis. سامانه مدیریت نشریات علمی, 19(4), 259-264. doi: 10.30476/dentjods.2018.41821
Ali Mahmoud Hashemi; Shiva Solahaye Kahnamouii; Hassan Aghajani; Khalil Frozannia; Alireza Pournasrollah; Rasoul Sadegh; Heidarali Esmaeeli; Yosef Ghadimi; Ebrahim Razmpa. "Quercetin Decreases Th17 Production by Down-Regulation of MAPK- TLR4 Signaling Pathway on T Cells in Dental Pulpitis". سامانه مدیریت نشریات علمی, 19, 4, 1397, 259-264. doi: 10.30476/dentjods.2018.41821
Mahmoud Hashemi, Ali, Solahaye Kahnamouii, Shiva, Aghajani, Hassan, Frozannia, Khalil, Pournasrollah, Alireza, Sadegh, Rasoul, Esmaeeli, Heidarali, Ghadimi, Yosef, Razmpa, Ebrahim. (1397). 'Quercetin Decreases Th17 Production by Down-Regulation of MAPK- TLR4 Signaling Pathway on T Cells in Dental Pulpitis', سامانه مدیریت نشریات علمی, 19(4), pp. 259-264. doi: 10.30476/dentjods.2018.41821
Mahmoud Hashemi, Ali, Solahaye Kahnamouii, Shiva, Aghajani, Hassan, Frozannia, Khalil, Pournasrollah, Alireza, Sadegh, Rasoul, Esmaeeli, Heidarali, Ghadimi, Yosef, Razmpa, Ebrahim. Quercetin Decreases Th17 Production by Down-Regulation of MAPK- TLR4 Signaling Pathway on T Cells in Dental Pulpitis. سامانه مدیریت نشریات علمی, 1397; 19(4): 259-264. doi: 10.30476/dentjods.2018.41821

Quercetin Decreases Th17 Production by Down-Regulation of MAPK- TLR4 Signaling Pathway on T Cells in Dental Pulpitis

Journal of Dentistry
مقاله 2، دوره 19، شماره 4، اسفند 2018، صفحه 259-264    اصل مقاله (318.1 K)
نوع مقاله: Original Article
شناسه دیجیتال (DOI): 10.30476/dentjods.2018.41821
نویسندگان
Ali Mahmoud Hashemi1؛ Shiva Solahaye Kahnamouii* 2؛ Hassan Aghajani3؛ Khalil Frozannia3؛ Alireza Pournasrollah4؛ Rasoul Sadegh4؛ Heidarali Esmaeeli5؛ Yosef Ghadimi5؛ Ebrahim Razmpa6
1Dental Implant Research Center, Tehran University of Medical Sciences, Tehran, Iran.
2Dept. of Oral and Maxillofacial Surgery, Tehran University of Medical Sciences, Tehran, Iran.
3Dept. of Cardiology, Tehran University of Medical Sciences, Tehran, Iran.
4Tabriz University of Medical Sciences, Tabriz, Iran.
5Dept. of Pathology, Tabriz University of Medical Sciences, Tabriz, Iran.
6Dept. of Otolaryngology, Tehran University of Medical Sciences, Tehran, Iran.
چکیده
Statement of the Problem: Quercetin is a pharmacological flavonoid that can inhibit high mobility group box1 (HMGB1) protein, a non-histone nuclear protein that is implicated in inflammation. Th17 cells are important cells in the pathogenesis of inflammation. Pulpitis is the inflammation of dental pulp, which usually is accompanied by pain. Quercetin may alleviate this inflammation.Purpose: The current study aimed to compare blocking of HMGB1 function and stimulation of HMGB1 function with quercetin and investigate the effects of the blockage on T helper 17 (Th17) cells and mitogen-activated protein kinase Toll-like receptor 4 (MAPK-TLR4) signaling pathway. Materials and Method: T cells isolated from the pulp involved with pulpitis and the normal pulp were cultured. The cells suspensions were plated in 6-wells culture plates and stimulated with 0.5 µg/ml of HMGB1 for 2, 4, 8, and 12 hours. For blocking TLR4, 10 µg/ml rabbit anti-human TLR4 antibody was added 1 hour before treatment with HMGB1. Results: The level of these cytokines decreased; moreover, western blot data showed that quercetin could decrease MAPK signaling pathway by means of inhibition of HMGB1 on T cells. The results showed the reduction of TLR4 pathway and Th17 cell polarization.Conclusion: Our results indicated that the levels of IL-17, IL-33, and IL-6 in supernatants from patients’ cultured T cells were increased after stimulation with HMGB-1 following employing quercetin. It also could inhibit MAPK signaling pathway, which subsequently could decrease Th17 production and IL-17. Quercetin could decrease pro-inflammatory cytokines and IL-17 production.
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