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    Anonymous
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    Ray Peat rekommenderar och pratar ofta om att apigenin och narangerin m fl är anti inflammatoriska ämnen som finns i tex citrus frukt. Hittade en artikel som faktiskt kollar på hår och apigenin och det visar sig att det skyddar hårsäckarna.

    Citron, Apelsin, Guava, m fl innehåller mkt av dessa amänen.

    Många bäckar små…

    “Treatment of [human epidermal keratinocytes] with dihydrotestosterone, which is known to be a primary factor of [androgenic alopecia], resulted in a concentration-dependent increase in TGF-beta1 promoter activity. However, treatment of HaCaT with the TGF-beta1 inhibitor, curcumin, resulted in a concentration-dependant decrease in TGF-beta1 expression. Subsequent use of this assay system to screen TGF-beta1 revealed that HaCaT that were treated with apigenin showed decreased levels of TGF-beta1 expression. In addition, treatment with apigenin also significantly increased the proliferation of both SV40T-DPCs (human Dermal Papilla Cells) and [human epidermal keratinocyte] cells. Furthermore, apigenin stimulated the elongation of hair follicles in a rat vibrissa hair follicle organ culture. Taken together, these findings suggest that apigenin, which is known to have antioxidant, anti-inflammatory, and anti-tumor properties, stimulates hair growth through downregulation of the TGF-beta1 gene.”

    http://www.ncbi.nlm.nih.gov/pubmed/19277688

    Lite annat som också visar att apigenin och andra flavonoids är anti inflammatoriska:

    “The results presented here suggest that the protective mechanism of apigenin may be attributed partly to decreased production of proinflammatory cytokines through the inhibition of COX-2 and NF-kB activation.”

    http://www.ncbi.nlm.nih.gov/pubmed/24958013

    “Here, we show that apigenin reduced lipopolysaccharide (LPS)-induced apoptosis by decreasing ROS production and the activity of caspase-3 in endothelial cells. Apigenin conferred protection against LPS-induced mitochondrial dysfunction and reestablished normal mitochondrial complex I activity, a major site of electron leakage and superoxide production, suggesting its ability to modulate endothelial cell metabolic function during inflammation.”

    http://www.ncbi.nlm.nih.gov/pubmed/23989609