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Ex vivo model exhibits protective effects of sesamin against destruction of cartilage induced with a combination of tumor necrosis factor-alpha and oncostatin M.

Khansai M, Boonmaleerat K, Pothacharoen P, Phitak T, Kongtawelert P - BMC Complement Altern Med (2016)

Bottom Line: Rheumatoid arthritis (RA) is an autoimmune disease associated with chronic inflammatory arthritis.Sesamin could be offering protection against cartilage degradation by reducing GAGs and collagen turnover in the generated model.Furthermore, the generated model revealed itself to be an impressive test model for the analysis of phytochemical substances against the cartilage degradation model for RA.

View Article: PubMed Central - PubMed

Affiliation: Thailand Excellence Center for Tissue Engineering and Stem Cells, Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.

ABSTRACT

Background: Rheumatoid arthritis (RA) is an autoimmune disease associated with chronic inflammatory arthritis. TNF-α and OSM are pro-inflammatory cytokines that play a key role in RA progression. Thus, reducing the effects of both cytokines is practical in order to relieve the progression of the disease. This current study is interested in sesamin, an active compound in sesame seeds. Sesamin has been shown to be a chondroprotective agent in osteoarthritis models. Here, we have evaluated a porcine cartilage explant as a cartilage degradation model related to RA induced by TNF-α and/or OSM in order to investigate the effects of sesamin on TNF-α and OSM in the cartilage degradation model.

Methods: A porcine cartilage explant was induced with a combination of TNF-α and OSM (test group) or IL-1β and OSM (control group) followed by a co-treatment of sesamin over a long-term period (35 days). After which, the tested explants were analyzed for indications of both the remaining and the degradation aspects using glycosaminoglycan and collagen as an indicator.

Results: The combination of TNF-α and OSM promoted cartilage degradation more than either TNF-α or OSM alone and was comparable with the combination of IL-1β and OSM. Sesamin could be offering protection against cartilage degradation by reducing GAGs and collagen turnover in the generated model.

Conclusions: Sesamin might be a promising agent as an alternative treatment for RA patients. Furthermore, the generated model revealed itself to be an impressive test model for the analysis of phytochemical substances against the cartilage degradation model for RA. The model could be used to test for the prevention of cartilage degradation in other biological agents induced with TNF-α and OSM as well.

No MeSH data available.


Related in: MedlinePlus

Histology staining; H&E staining for chondrocyte cell morphology, Safranin O staining for S-GAGs in cartilage (red color) and immunohistochemistry staining for type ΙΙ collagen remaining in the cartilage (brown color) (x400). a Histology staining of cytokine(s)-induced conditions. b Histology staining of co-treatment of TNF-α and OSM induced-condition with sesamin
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Fig6: Histology staining; H&E staining for chondrocyte cell morphology, Safranin O staining for S-GAGs in cartilage (red color) and immunohistochemistry staining for type ΙΙ collagen remaining in the cartilage (brown color) (x400). a Histology staining of cytokine(s)-induced conditions. b Histology staining of co-treatment of TNF-α and OSM induced-condition with sesamin

Mentions: The important evidence that supported the chondroprotective effects of sesamin against TNF-α/OSM-induced cartilage degradation came from a histological examination (Fig. 6a). TNF-α/OSM and IL-1β/OSM caused severe cartilage damage when compared with other conditions, which was observed due to the cartilage’s abnormal appearance (Fig. 6a). Additionally, the chondrocytes seemed unhealthy when compared with the normal specimens in the control group. Moreover, the surface of the cartilage explants when under the induced condition seemed decomposed. However, the presence of sesamin in the induction system resulted in better chondrocyte cell morphology and a healthy appearance of the cartilage, which was similar to results found in the dexamethasone treatment (Fig. 6b). Furthermore, the results clearly indicated that the induction with TNF-α in combination with OSM caused a severe loss of S-GAGs in the cartilage as same as IL-1β and OSM. The presence of sesamin could protect S-GAGs from depletion in both combinations of cytokine-induced cartilage. Although, in the TNF-α/OSM treatment, the lower concentration value of sesamin seemed to maintain S-GAGs more effectively than was found with the higher concentration value of sesamin (Fig. 6b). For type ΙΙ collagen content, the long-term induction of cartilage with TNF-α and OSM caused a severe loss of collagen (Fig. 6). Notably, collagen that was co-cultured with sesamin was protected from depletion when sesamin was introduced in a dose-dependent manner (Fig. 6b). However, the protective effects of sesamin were shown to be less than those of the dexamethasone treatment.Fig. 6


Ex vivo model exhibits protective effects of sesamin against destruction of cartilage induced with a combination of tumor necrosis factor-alpha and oncostatin M.

Khansai M, Boonmaleerat K, Pothacharoen P, Phitak T, Kongtawelert P - BMC Complement Altern Med (2016)

Histology staining; H&E staining for chondrocyte cell morphology, Safranin O staining for S-GAGs in cartilage (red color) and immunohistochemistry staining for type ΙΙ collagen remaining in the cartilage (brown color) (x400). a Histology staining of cytokine(s)-induced conditions. b Histology staining of co-treatment of TNF-α and OSM induced-condition with sesamin
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4940911&req=5

Fig6: Histology staining; H&E staining for chondrocyte cell morphology, Safranin O staining for S-GAGs in cartilage (red color) and immunohistochemistry staining for type ΙΙ collagen remaining in the cartilage (brown color) (x400). a Histology staining of cytokine(s)-induced conditions. b Histology staining of co-treatment of TNF-α and OSM induced-condition with sesamin
Mentions: The important evidence that supported the chondroprotective effects of sesamin against TNF-α/OSM-induced cartilage degradation came from a histological examination (Fig. 6a). TNF-α/OSM and IL-1β/OSM caused severe cartilage damage when compared with other conditions, which was observed due to the cartilage’s abnormal appearance (Fig. 6a). Additionally, the chondrocytes seemed unhealthy when compared with the normal specimens in the control group. Moreover, the surface of the cartilage explants when under the induced condition seemed decomposed. However, the presence of sesamin in the induction system resulted in better chondrocyte cell morphology and a healthy appearance of the cartilage, which was similar to results found in the dexamethasone treatment (Fig. 6b). Furthermore, the results clearly indicated that the induction with TNF-α in combination with OSM caused a severe loss of S-GAGs in the cartilage as same as IL-1β and OSM. The presence of sesamin could protect S-GAGs from depletion in both combinations of cytokine-induced cartilage. Although, in the TNF-α/OSM treatment, the lower concentration value of sesamin seemed to maintain S-GAGs more effectively than was found with the higher concentration value of sesamin (Fig. 6b). For type ΙΙ collagen content, the long-term induction of cartilage with TNF-α and OSM caused a severe loss of collagen (Fig. 6). Notably, collagen that was co-cultured with sesamin was protected from depletion when sesamin was introduced in a dose-dependent manner (Fig. 6b). However, the protective effects of sesamin were shown to be less than those of the dexamethasone treatment.Fig. 6

Bottom Line: Rheumatoid arthritis (RA) is an autoimmune disease associated with chronic inflammatory arthritis.Sesamin could be offering protection against cartilage degradation by reducing GAGs and collagen turnover in the generated model.Furthermore, the generated model revealed itself to be an impressive test model for the analysis of phytochemical substances against the cartilage degradation model for RA.

View Article: PubMed Central - PubMed

Affiliation: Thailand Excellence Center for Tissue Engineering and Stem Cells, Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.

ABSTRACT

Background: Rheumatoid arthritis (RA) is an autoimmune disease associated with chronic inflammatory arthritis. TNF-α and OSM are pro-inflammatory cytokines that play a key role in RA progression. Thus, reducing the effects of both cytokines is practical in order to relieve the progression of the disease. This current study is interested in sesamin, an active compound in sesame seeds. Sesamin has been shown to be a chondroprotective agent in osteoarthritis models. Here, we have evaluated a porcine cartilage explant as a cartilage degradation model related to RA induced by TNF-α and/or OSM in order to investigate the effects of sesamin on TNF-α and OSM in the cartilage degradation model.

Methods: A porcine cartilage explant was induced with a combination of TNF-α and OSM (test group) or IL-1β and OSM (control group) followed by a co-treatment of sesamin over a long-term period (35 days). After which, the tested explants were analyzed for indications of both the remaining and the degradation aspects using glycosaminoglycan and collagen as an indicator.

Results: The combination of TNF-α and OSM promoted cartilage degradation more than either TNF-α or OSM alone and was comparable with the combination of IL-1β and OSM. Sesamin could be offering protection against cartilage degradation by reducing GAGs and collagen turnover in the generated model.

Conclusions: Sesamin might be a promising agent as an alternative treatment for RA patients. Furthermore, the generated model revealed itself to be an impressive test model for the analysis of phytochemical substances against the cartilage degradation model for RA. The model could be used to test for the prevention of cartilage degradation in other biological agents induced with TNF-α and OSM as well.

No MeSH data available.


Related in: MedlinePlus