Amelioration of adjuvant-induced arthritis by ursolic acid through altered Th1/Th2 cytokine production

Ahmad, Sheikh F.; Khan, Beenish; Bani, Sarang; Suri, Krishna; Satti, Naresh K.; Qazi, Ghulam N.

doi:10.1016/j.phrs.2005.11.005

Cited by 56 publications

(34 citation statements)

References 18 publications

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“…UA confers its anti-inflammatory activities through a number of different mechanisms, including inhibiting the production of proinflammatory cytokines such as IL-2, IFN-γ, and TNF-α [19] , prostaglandin E2 [20] , and cyclooxygenase 2. Earlier studies suggested that the anti-inflammatory properties of UA were mediated by the suppression of nuclear factor (NF)-κB, a major transcription factor that regulates the expression of multiple proinflammatory cytokines [12,21] .…”

Section: Discussionmentioning

confidence: 99%

Ursolic acid ameliorates autoimmune arthritis via suppression of Th17 and B cell differentiation

Baek

Lee

et al. 2014

Acta Pharmacol Sin

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Aim: Ursolic acid (UA) is a pentacyclic triterpenoid found in most plant species, which has been shown anti-inflammatory and antioxidative activities. In this study, we examined the effects of UA on collagen-induced arthritis (CIA) in mice, and to identify the mechanisms underlying the effects. Methods: CIA was induced in mice. Two weeks later, the mice were treated with UA (150 mg/kg, ip, 3 times per week) for 4 weeks. The expression of cytokines and oxidative stress markers in joint tissues was measured with immunohistochemistry. The numbers of CD4 + IL-17 + , CD4 + CD25 + Foxp3 + and pSTAT3 cells in spleens were determined using confocal immunostaining or flowcytometric analyses. Serum antibody levels and B cell-associated marker mRNAs were analyzed with ELISAs and qRT-PCR, respectively. CD4 + T cells and CD19 + B cells were purified from mice spleens for in vitro studies. Results: UA treatment significantly reduced the incidence and severity of CIA-induced arthritis, accompanied by decreased expression of proinflammatory cytokines (TNF-α, IL-1β, IL-6, IL-21 and IL-17) and oxidative stress markers (nitrotyrosine and iNOS) in arthritic joints. In CIA mice, UA treatment significantly decreased the number of Th17 cells, while increased the number of Treg cells in the spleens, which was consistent with decreased expression of pSTAT3, along with IL-17 and RORγt in the splenocytes. In addition, UA treatment significantly reduced the serum CII-specific IgG levels in CIA mice. The inhibitory effects of UA on Th17 cells were confirmed in an in vitro model of Th17 differentiation. Furthermore, UA dose-dependently suppressed the expression of B cell-associated markers Bcl-6, Blimp1 and AID mRNAs in purified CD19 + B cells pretreated with IL-21 or LPS in vitro. Conclusion: UA treatment significantly ameliorates CIA in mice via suppression of Th17 and differentiation. By targeting pathogenic Th17 cells and autoantibody production, UA may be useful for the treatment of autoimmune arthritis and other Th17-related diseases.

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Section: Discussionmentioning

confidence: 99%

Ursolic acid ameliorates autoimmune arthritis via suppression of Th17 and B cell differentiation

Baek

Lee

et al. 2014

Acta Pharmacol Sin

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“…It has also been proved that ursolic acid has membrane stabilizing and radical scavenging activity (Han et al, 1997;Balanehru & Nagarajan, 1992). Recently, it has been reported that ursolic acid ameliorates adjuvant induced arthritis through distorted Th1/Th2 cytokine production (Ahmad et al, 2006) and also improves the GSH and CAT levels (Saravanan & Viswanathan, 2006;Kitani et al, 1999). Hence, it is suggested that presence of these phytoconstituents might be responsible for the bolstering of antioxidant defense system in CFA group, thereby precluding arthritis.…”

Section: Discussionmentioning

confidence: 99%

Antioxidant potential ofGaultheria fragrantissimaagainst adjuvant induced arthritis in Wistar rats

Shanmugarajan

Maity

Somasundaram

et al. 2009

Pharmaceutical Biology

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“…UA was also found to inhibit tumor growth and accentuate the survival rate of mice by decreasing inflammation-inducing mediators (i.e., STAT3, AKT, and IKKa/b) [60]. In addition, when arthritic BALB/c mice were treated with UA, the production of pro-inflammatory cytokines (e.g., IL-2, IFN-γ, and TNF-) by Th-1 cells was reduced [59]. Takada et al found that in human umbilical vein endothelial cells (HUVECs), UA causes a decrease in the expression of E-selectin via the inhibition of NF-κB translocation to the nucleus [61].…”

Section: Figurementioning

confidence: 94%

“…(e.g., IL-2, IFN-γ, and TNF-α) by Th-1 cells after the use of UA in vivo [59]. UA was also found to inhibit tumor growth and accentuate the survival rate of mice by decreasing inflammation-inducing mediators (i.e., STAT3, AKT, and IKKa/b) [60].…”

Section: Figurementioning

confidence: 94%

Therapeutic Interventions Using Ursolic Acid for Cancer Treatment

Ray¹,

Kim²

2016

Med chem

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Amelioration of adjuvant-induced arthritis by ursolic acid through altered Th1/Th2 cytokine production

Cited by 56 publications

References 18 publications

Ursolic acid ameliorates autoimmune arthritis via suppression of Th17 and B cell differentiation

Ursolic acid ameliorates autoimmune arthritis via suppression of Th17 and B cell differentiation

Antioxidant potential ofGaultheria fragrantissimaagainst adjuvant induced arthritis in Wistar rats

Therapeutic Interventions Using Ursolic Acid for Cancer Treatment

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