Limits...
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

Treatment with chebulanin ameliorated the clinical severity of CIA.CIA was induced, and after the onset of arthritis animals were treated with vehicle (control) or chebulanin (at 40 mg/kg, 80 mg/kg or 160 mg/kg) daily for 28 days. Severity of arthritis was evaluated every two days. Error bars represent the standard deviation (n = 6); * p <0.05 vs. untreated CIA mice.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4581703&req=5

pone.0139052.g001: Treatment with chebulanin ameliorated the clinical severity of CIA.CIA was induced, and after the onset of arthritis animals were treated with vehicle (control) or chebulanin (at 40 mg/kg, 80 mg/kg or 160 mg/kg) daily for 28 days. Severity of arthritis was evaluated every two days. Error bars represent the standard deviation (n = 6); * p <0.05 vs. untreated CIA mice.

Mentions: A total of 30 male DBA/1 mice were randomly divided into the following five groups (with six animals (n = 6) in each group): normal group = normal mice; CIA group = collagen-induced arthritis mice; low-dose group = chebulanin 40 mg/kg-treated CIA mice; mid-dose group = chebulanin 80 mg/kg-treated CIA mice; high-dose group = chebulanin 160 mg/kg-treated CIA mice. The dose and the route of chebulanin administration used in this study were chosen on the basis of preliminary experiments. CIA in mice was achieved as described by Brand et al [21]. Briefly, all mice outside the normal group were administered a dose of bovine type II collagen (100 μg) emulsified with complete Freund’s adjuvant intradermally at the base of the tail. Animals received a booster injection of bovine type II collagen (100 μg) emulsified with incomplete Freund’s adjuvant 21 days after the initial immunization. The chebulalin was dissolved in 1% sodium carboxyl methyl cellulose (1% CMC-Na water solution) and administered intragastrically once daily starting at two-and-a-half weeks (day 39) after the booster injection (after full development of CIA) for a duration of 28 days. The normal and the CIA groups received a 1% CMC solution administered in the same manner as a control. Mice were observed for two more weeks after administration and sacrificed by cervical dislocation at the end of experimentation (a total of 80 days). A time line diagram of flow chart can be seen in result part (Fig 1). Ankle joints in the paw were removed and fixed in 10% neutral buffered formalin.


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)

Treatment with chebulanin ameliorated the clinical severity of CIA.CIA was induced, and after the onset of arthritis animals were treated with vehicle (control) or chebulanin (at 40 mg/kg, 80 mg/kg or 160 mg/kg) daily for 28 days. Severity of arthritis was evaluated every two days. Error bars represent the standard deviation (n = 6); * p <0.05 vs. untreated CIA mice.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0139052.g001: Treatment with chebulanin ameliorated the clinical severity of CIA.CIA was induced, and after the onset of arthritis animals were treated with vehicle (control) or chebulanin (at 40 mg/kg, 80 mg/kg or 160 mg/kg) daily for 28 days. Severity of arthritis was evaluated every two days. Error bars represent the standard deviation (n = 6); * p <0.05 vs. untreated CIA mice.
Mentions: A total of 30 male DBA/1 mice were randomly divided into the following five groups (with six animals (n = 6) in each group): normal group = normal mice; CIA group = collagen-induced arthritis mice; low-dose group = chebulanin 40 mg/kg-treated CIA mice; mid-dose group = chebulanin 80 mg/kg-treated CIA mice; high-dose group = chebulanin 160 mg/kg-treated CIA mice. The dose and the route of chebulanin administration used in this study were chosen on the basis of preliminary experiments. CIA in mice was achieved as described by Brand et al [21]. Briefly, all mice outside the normal group were administered a dose of bovine type II collagen (100 μg) emulsified with complete Freund’s adjuvant intradermally at the base of the tail. Animals received a booster injection of bovine type II collagen (100 μg) emulsified with incomplete Freund’s adjuvant 21 days after the initial immunization. The chebulalin was dissolved in 1% sodium carboxyl methyl cellulose (1% CMC-Na water solution) and administered intragastrically once daily starting at two-and-a-half weeks (day 39) after the booster injection (after full development of CIA) for a duration of 28 days. The normal and the CIA groups received a 1% CMC solution administered in the same manner as a control. Mice were observed for two more weeks after administration and sacrificed by cervical dislocation at the end of experimentation (a total of 80 days). A time line diagram of flow chart can be seen in result part (Fig 1). Ankle joints in the paw were removed and fixed in 10% neutral buffered formalin.

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