L-Ascorbic acid sodium salt (Sodium ascorbate) functions as an electron donor and serves as an endogenous antioxidant. This compound specifically inhibits Cav3.2 channels with an IC50 of 6.5 μM, and it is noted for its roles in enhancing collagen deposition and inhibiting elastogenesis[1].[2].[3].
体内研究
In studies involving transgenic (Tg) rats, those treated with L-Ascorbic acid sodium salt exhibit a higher incidence of carcinoma (29.6%) compared to those not receiving the treatment (15.4%). These findings suggest that the presence of L-Ascorbic acid sodium salt influences carcinoma development, although transgenic rats generally show a predisposition to develop malignant tumors in various organs, regardless of the treatment[5].
After a 12-week treatment with PEITC, all animals develop either simple hyperplasia or papillary or nodular (PN) hyperplasia, which largely resolves by the 48-week mark, independent of any L-Ascorbic acid sodium salt treatment. However, following 24 weeks of PEITC treatment, some of these lesions progress to dysplasia and carcinoma, although by week 48, only a small number of cases show such advancement. The enhancement effect of L-Ascorbic acid sodium salt treatment is particularly noticeable in the progression of simple and PN hyperplasias in rats[6].
体外研究
Research indicates that the conditioned medium from B16F10 cells can significantly prevent cell apoptosis induced by L-Ascorbic acid sodium salt (Sodium ascorbate) at a concentration of 10 mM. The active components in the medium are identified to have a relative molecular mass below 5,000[4].
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