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Anti-Arthritic Effect of Chebulanin on Collagen-Induced Arthritis in Mice.

Zhao Y, Liu F, Liu Y, Zhou D, Dai Q, Liu S - PLoS ONE (2015)

Bottom Line: To date, there are no effective therapies to slow the progress of this degenerative condition.Furthermore, micro-CT analysis revealed that chebulanin induced a dose-dependent reduction in cartilage destruction and bone erosion.Therefore, chebulanin is a strong therapeutic alternative for the treatment of RA.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacy, Southwest Hospital, Third Military Medical University, Chongqing, China.

ABSTRACT
Rheumatoid arthritis is a chronic degenerative autoimmune disease characterized by persistent inflammation of synovial membranes, which leads to cartilage destruction and bone erosion. To date, there are no effective therapies to slow the progress of this degenerative condition. Here, we evaluate the anti-arthritic effect of chebulanin, an abundant anti-inflammatory agent isolated from Terminalia chebula, in collagen induced arthritis in DBA/1 mice by intragastric administration. Arthritic severity was scored by performing histopathological evaluation of the joints and measuring the expression of inflammatory cytokines and relative enzymes by immunohistochemical staining. In parallel, bone destruction and erosion were confirmed by micro-CT. Our data revealed that chebulanin significantly improved the severity of arthritis. Specifically, the histopathological characteristics of the tissues were improved and expression of TNF-α, IL-6, MMP-3 and COX-2 in the paws and joints of the treated mice decreased in a dose-dependent manner compared with control mice. Furthermore, micro-CT analysis revealed that chebulanin induced a dose-dependent reduction in cartilage destruction and bone erosion. Taken together, our findings suggest that chebulanin suppresses the expression of inflammatory mediators and prevents cartilage destruction and bone erosion in mice. Therefore, chebulanin is a strong therapeutic alternative for the treatment of RA.

No MeSH data available.


Related in: MedlinePlus

Chebulanin suppresses CIA in mice by different mechanisms.Chebulanin treatment ameliorates collagen-induced arthritis by inhibiting the expression of pro-inflammatory cytokines (TNF-α, IL-6), cyclooxygenase (COX-2) and matrix metalloproteinases (MMP-3).
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pone.0139052.g007: Chebulanin suppresses CIA in mice by different mechanisms.Chebulanin treatment ameliorates collagen-induced arthritis by inhibiting the expression of pro-inflammatory cytokines (TNF-α, IL-6), cyclooxygenase (COX-2) and matrix metalloproteinases (MMP-3).

Mentions: The fruits of TC have been widely used in many Asian countries as a traditional folk medicine for treating cough or diarrhea. The TC bioactive constituents include the polyphenols chebulagic acid, chebulinic acid, chebulanin and gallic acid [17], which have anti-oxidant [12], anti-inflammatory [13, 14], anti-bacterial [15] and anti-arthritic properties [16]. Previously, we demonstrated the in vitro anti-oxidative and anti-inflammatory properties of the chebulanin polyphenol. In this study, we show that oral administration of chebulanin to CIA mice efficiently alleviates the severity of arthritic bone features. The mean arthritis score in our chebulanin-treated CIA mice was found to be significantly lower than that of the untreated CIA mice, especially at doses of 80 mg/kg and 160 mg/kg. In addition, chebulanin significantly improved the CIA-related histopathological changes through a mechanism involving decreasing the expression of inflammatory cytokines (TNF-α, IL-6) and inflammation-associated enzymes (COX-2, MMP-3) in joint tissues. Importantly, no important adverse effects were observed in the mice following the chebulanin treatment. In summary, we show for the first time that chebulanin has therapeutic potential for the treatment of RA based upon our observations that it can improve CIA by suppressing inflammatory mediator release and preventing cartilage and bone destruction (Fig 7).


Anti-Arthritic Effect of Chebulanin on Collagen-Induced Arthritis in Mice.

Zhao Y, Liu F, Liu Y, Zhou D, Dai Q, Liu S - PLoS ONE (2015)

Chebulanin suppresses CIA in mice by different mechanisms.Chebulanin treatment ameliorates collagen-induced arthritis by inhibiting the expression of pro-inflammatory cytokines (TNF-α, IL-6), cyclooxygenase (COX-2) and matrix metalloproteinases (MMP-3).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4581703&req=5

pone.0139052.g007: Chebulanin suppresses CIA in mice by different mechanisms.Chebulanin treatment ameliorates collagen-induced arthritis by inhibiting the expression of pro-inflammatory cytokines (TNF-α, IL-6), cyclooxygenase (COX-2) and matrix metalloproteinases (MMP-3).
Mentions: The fruits of TC have been widely used in many Asian countries as a traditional folk medicine for treating cough or diarrhea. The TC bioactive constituents include the polyphenols chebulagic acid, chebulinic acid, chebulanin and gallic acid [17], which have anti-oxidant [12], anti-inflammatory [13, 14], anti-bacterial [15] and anti-arthritic properties [16]. Previously, we demonstrated the in vitro anti-oxidative and anti-inflammatory properties of the chebulanin polyphenol. In this study, we show that oral administration of chebulanin to CIA mice efficiently alleviates the severity of arthritic bone features. The mean arthritis score in our chebulanin-treated CIA mice was found to be significantly lower than that of the untreated CIA mice, especially at doses of 80 mg/kg and 160 mg/kg. In addition, chebulanin significantly improved the CIA-related histopathological changes through a mechanism involving decreasing the expression of inflammatory cytokines (TNF-α, IL-6) and inflammation-associated enzymes (COX-2, MMP-3) in joint tissues. Importantly, no important adverse effects were observed in the mice following the chebulanin treatment. In summary, we show for the first time that chebulanin has therapeutic potential for the treatment of RA based upon our observations that it can improve CIA by suppressing inflammatory mediator release and preventing cartilage and bone destruction (Fig 7).

Bottom Line: To date, there are no effective therapies to slow the progress of this degenerative condition.Furthermore, micro-CT analysis revealed that chebulanin induced a dose-dependent reduction in cartilage destruction and bone erosion.Therefore, chebulanin is a strong therapeutic alternative for the treatment of RA.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacy, Southwest Hospital, Third Military Medical University, Chongqing, China.

ABSTRACT
Rheumatoid arthritis is a chronic degenerative autoimmune disease characterized by persistent inflammation of synovial membranes, which leads to cartilage destruction and bone erosion. To date, there are no effective therapies to slow the progress of this degenerative condition. Here, we evaluate the anti-arthritic effect of chebulanin, an abundant anti-inflammatory agent isolated from Terminalia chebula, in collagen induced arthritis in DBA/1 mice by intragastric administration. Arthritic severity was scored by performing histopathological evaluation of the joints and measuring the expression of inflammatory cytokines and relative enzymes by immunohistochemical staining. In parallel, bone destruction and erosion were confirmed by micro-CT. Our data revealed that chebulanin significantly improved the severity of arthritis. Specifically, the histopathological characteristics of the tissues were improved and expression of TNF-α, IL-6, MMP-3 and COX-2 in the paws and joints of the treated mice decreased in a dose-dependent manner compared with control mice. Furthermore, micro-CT analysis revealed that chebulanin induced a dose-dependent reduction in cartilage destruction and bone erosion. Taken together, our findings suggest that chebulanin suppresses the expression of inflammatory mediators and prevents cartilage destruction and bone erosion in mice. Therefore, chebulanin is a strong therapeutic alternative for the treatment of RA.

No MeSH data available.


Related in: MedlinePlus