JavaScript seems to be disabled in your browser. For the best experience on our site, be sure to turn on Javascript in your browser.
Tel: +1-832-696-8203
Email: [email protected]
Worldwide Distributors
In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
Cell lines
Primary human sebocytes
Reaction Conditions
7 ~ 14 d incubation
Applications
Isotretinoin decreased sebocyte proliferation in a dose- and time-dependent manner, with IC50 values being 10 μM after a 7-d incubation and 1 μM after a 14-d incubation, respectively. Isotretinoin (8 d) also inhibited the synthesis of triglycerides, wax/stearyl esters and free fatty acids, and modulated keratin expression in primary human sebocytes at a concentration of 0.1 μM.
Animal models
Male inbred Lewis (LEW, RT11) and Fisher (F344, RT11v1) rats, 200 ~ 220 g
Dosage form
2 mg/kg/day
Administered orally for 8 weeks
Isotretinoin reduced chronic rejection damage and decreased mRNA expression of IFN-γ and IL-10 in allografts in chronic Fisher344?Lewis transplant mice, an allograft nephropathy model. Thus, isotretinoin could serve as a potent immunosuppressive and anti-fibrotic agent able to prevent and inhibit progression of chronic allograft nephropathy.
Note
The technical data provided above is for reference only.
References:
1. Zouboulis CC, Korge B, Akamatsu H, et al. Effects of 13-cis-retinoic acid, all-trans-retinoic acid, and acitretin on the proliferation, lipid synthesis and keratin expression of cultured human sebocytes in vitro. Journal of Investigative Dermatology, 1991, 96(5): 792-797.
2. Adams J, Kiss E, Arroyo AB, et al. 13-cis retinoic acid inhibits development and progression of chronic allograft nephropathy. The American Journal of Pathology, 2005, 167(1): 285-298.