Amelioration of autoimmune arthritis by naringin through modulation of T regulatory cells and Th1/Th2 cytokines.
Naringin, a well-known flavanone glycoside found in grapefruit and other citrus fruits, was determined to be an effective anti-inflammatory compound. We investigated the effect of naringin on the key mediators of arthritic inflammation, namely T cell subsets, CD4(+)GITR(+) expressing cells, CD4(+)CD25(+)Foxp3(+) (Treg), Th1/Th2 cytokines and inflammatory mediators. We treated Balb/c mice (p.o.) with naringin (20, 40 and 80 mg/kg) for 14 days. Compared with the vehicle-treated and arthritic-control mice, the naringin treatment demonstrated a considerable decrease in the level of T cells, CD4(+)GITR(+), Th1 cytokine and inflammatory mediator expressions. In contrast, naringin treatment resulted in significantly up-regulated Treg and Th2 cytokine levels. Therefore, the naringin-induced inhibition of the T cells, various pro-inflammatory cytokines and inflammatory mediators that facilitate cellular infiltration into the joints might have contributed to its anti-arthritic activity. Our data suggest that naringin diminished the AIA in mice and it could be a potential alternative/adjunct treatment for RA.
Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, PO Box 11451, Riyadh, Saudi Arabia. Electronic address: s_fayazahmad@yahoo.com.
Sheikh Fayaz
SF
Ahmad
Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, PO Box 11451, Riyadh, Saudi Arabia; Department of Cell Biology, National Research Centre, Cairo, Egypt.
Khairy M A
KM
Zoheir
Department of Pathology, Faculty of Medicine (Girls), Al-Azhar University, Cairo, Egypt.
Hala E
HE
Abdel-Hamied
Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, PO Box 11451, Riyadh, Saudi Arabia.
Abdelkader E
AE
Ashour
Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, PO Box 11451, Riyadh, Saudi Arabia.
Saleh A
SA
Bakheet
Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, PO Box 11451, Riyadh, Saudi Arabia; Department of Pharmacology and Toxicology, College of Pharmacy, Al-Azhar University, Cairo, Egypt.
Sabry M
SM
Attia
Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, PO Box 11451, Riyadh, Saudi Arabia; Department of Pharmacology and Toxicology, College of Pharmacy, Al-Azhar University, Cairo, Egypt.
Adel R A
AR
Abd-Allah
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D001168:Arthritis / Q000276:immunology / Q000628:therapy*; D001327:Autoimmune Diseases / Q000276:immunology / Q000628:therapy*; D015704:CD4 Antigens / Q000378:metabolism; D002478:Cells, Cultured; D032083:Citrus paradisi / Q000737:chemistry*; D016207:Cytokines / Q000378:metabolism; D018450:Disease Progression; D005260:Female; D044950:Flavanones / Q000627:therapeutic use*; D051858:Forkhead Transcription Factors / Q000378:metabolism; D053450:Glucocorticoid-Induced TNFR-Related Protein / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism; D053645:Interleukin-2 Receptor alpha Subunit / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D016176:T-Lymphocyte Subsets / Q000187:drug effects* / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects* / Q000276:immunology; D058408:Th1-Th2 Balance
D000894:Anti-Inflammatory Agents, Non-Steroidal; D015704:CD4 Antigens; D016207:Cytokines; D044950:Flavanones; D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D053450:Glucocorticoid-Induced TNFR-Related Protein; D018836:Inflammation Mediators; D053645:Interleukin-2 Receptor alpha Subunit; C106544:Tnfrsf18 protein, mouse; C005274:naringin
Adjuvant induced arthritis; Inflammatory mediators; Mouse model; Naringin; T cell subsets; Treg cells