Dehydrocorydaline chloride

Research use only, not for human use.

Dehydrocorydaline chloride is an alkaloid with anti-inflammatory and anti-cancer activity. Can improve the activation of p38 MAPK.

Dehydrocorydaline chloride is an alkaloid with anti-inflammatory and anti-cancer activity. Can improve the activation of p38 MAPK.Treatment of C2C12 myoblasts with 500 nM dehydrocorydrine increased the expression level of muscle-specific proteins (including MyoD, myogenin and myosin heavy chain). Treatment with dehydrocorydrine can increase p38 MAPK activation and the interaction between MyoD and E protein. In addition, the treatment of dehydrohydroxyproline can restore the defects of differentiation-induced p38 MAPK activation and differentiation of myoblasts in C2C12 myoblasts induced by the differentiated early growth receptor protein Cdo. Dehydrohydroxyproline significantly inhibits the proliferation of MCF-7 cells in a dose-dependent manner, which can be reversed by the caspase-8 inhibitor Z-IETD-FMK. Dehydrohydroxyproline increases DNA fragments without affecting ΔΨm. Western blot analysis showed that dehydrocorydrine increased dose-dependently Bax protein expression and decreased Bcl-2 protein expression. In addition, dehydrohydroxyproline induces caspase-7,-8 activation and PARP cleavage without affecting caspase-9. These results indicate that dehydrohydroxyproline inhibits the proliferation of MCF-7 cells by inducing apoptosis by regulating Bax/Bcl-2, activating caspase and cleaving PARP.Dehydrocobaltate (3.6, 6 or 10 mg/kg, intraperitoneal injection) showed a dose-dependent anti-nociceptive effect in the acetic acid-induced writhing test and significantly reduced formalin-induced mice Pain reaction. In the formalin test, dehydrocorydrine can reduce the expression of caspase 6 (CASP6), TNF-α, IL-1β and IL-6 proteins in the spinal cord. It was confirmed that dehydroyanhusine has an analgesic effect on mice.

Treatment of C2C12 myoblasts with 500 nM Dehydrocorydaline increases the expression levels of muscle-specific proteins, including MyoD, myogenin and myosin heavy chain. Treatment with Dehydrocorydaline elevates p38 MAPK activation and the interaction of MyoD with an E protein. Furthermore, defects in differentiation-induced p38 MAPK activation and myoblast differentiation induced by depletion of the promyogenic receptor protein Cdo in C2C12 myoblasts are restored by Dehydrocorydaline treatment. Dehydrocorydaline significantly inhibits MCF-7 cell proliferation in a dose- dependent manner, which can be reversed by a caspase-8 inhibitor, Z-IETD-FMK. Dehydrocorydaline increases DNA fragments without affecting ΔΨm. Western blotting assay shows that dehydrocorydaline dose-dependently increases Bax protein expression and decreases Bcl-2 protein expression. Furthermore, dehydrocorydaline induces activation of caspase-7,-8 and the cleavage of PARP without affecting caspase-9. These results show that dehydrocorydaline inhibits MCF-7 cell proliferation by inducing apoptosis mediated by regulating Bax/Bcl-2, activating caspases as well as cleaving PARP.

Dehydrocorydaline (3.6, 6 or 10 mg/kg, i.p.) shows a dose-dependent antinociceptive effect in the acetic acid-induced writhing test and significantly attenuates the formalin-induced pain responses in mice. In the formalin test, dehydrocorydaline decreases the expression of caspase 6 (CASP6), TNF-α, IL-1β and IL-6 proteins in the spinal cord. These findings confirm that Dehydrocorydaline has antinociceptive effects in mice.

13-Methylpalmatine chloride

MAPK/ERK Signaling

p38 MAPK

p38 MAPK|Bax|Bcl-2|caspase-7|caspase-8|PARP

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10605-03-5

401.88

C22H24ClNO4

>98% (HPLC)

DMSO:24 mg/mL(59.72 mM)

[Cl-].COc1cc2CC[n+]3cc4c(OC)c(OC)ccc4c(C)c3-c2cc1OC

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(-20℃)

With Ice Pack

≥ 2 years