Comparison between the effect of kartogenin and TGFβ3 on chondrogenesis of human adipose- derived stem cells in fibrin scaffold.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Due to very sluggish turnover at the molecular and cellular level, the healing of chondral damages has been considered difficult. In the current study, the effects of the Kartogenin, a small heterocyclic molecule on chondrogenic differentiation of stem cells was compared to TGF-β3. Human Adipose-Derived Stem Cells were extracted during an elective surgery. Cell viability was estimated by MTT assay, differentiated cells evaluated by histological and immunohistochemical techniques. Expression of cartilage specific genes (SOX9, Aggrecan, type II and X collagens) assessed by real-time PCR. The real-time PCR assay has revealed the expression of gene marker of chondrogenesis, SOX9, Aggrecan and type II collagen, both in Kartogenin and TGFβ3 groups compared to the control group, significantly (p < 0.05). A low expression level of collagen type X as a hypertrophic marker was seen in cartilage produced by using Kartogenin. Meanwhile, the level of type X collagen protein in Kartogenin group was significantly decreased (p > 0.05) compared to TGF-β3 group. Kartogenin was suitable for successful chondrogenic differentiation of human adipose- derived stem cells and a suppressor of the consequent hypertrophy (Tab. 1, Fig. 5, Ref. 31).

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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