Chelerythrine Chloride is a cell-permeable inhibitor of protein kinase C, competitive with respect to the phosphate acceptor and non-competitive with respect to ATP.

PKC:660 nM.

Chelerythrine通过IC50为1.5 μM的浓度抑制BclXL-Bak BH3肽的结合，并且能够将含BH3的蛋白Bax从BclXL中排斥出去。处理有Chelerythrine的哺乳动物细胞会发生凋亡，其特征表明了线粒体途径的参与[1]。此外，Chelerythrine处理能通过选择性抑制p38丝裂原活化蛋白激酶（MAPK）和细胞外信号调节激酶1及2（ERK1/2）的激活，从而抑制LPS诱导的小鼠腹腔巨噬细胞中TNF-α水平和NO产生。Chelerythrine对NO和TNF-α细胞因子产生的效应可能通过p38 MAPK和ERK1/2在炎症介质表达调控中的作用来解释[2]。Chelerythrine对人类单核细胞白血病细胞表现出细胞毒性作用，LD50值为3.46 μM。LPS刺激后两小时，受sanguinarine和Chelerythrine影响的细胞CCL-2表达显著下降了3.5倍和1.9倍[3]。Chelerythrine chloride能显著以剂量依赖方式增强ERK1/2的磷酸化，同时抑制p38的磷酸化[4]。

Chelerythrine在实验性诱导的小鼠内毒素休克模型中显示出显著的抗炎效果，其机制为通过抑制LPS诱导的血清中肿瘤坏死因子-α（TNF-α）水平和一氧化氮（NO）的产生来实现[2]。Chelerythrine Chloride（每天5 mg/kg，腹腔注射）能够诱导RCC细胞的凋亡，而对小鼠无显著毒性。Chelerythrine Chloride处理以剂量依赖的方式导致p53的积累[4]。

Chelerythrine is dissolved in DMSO. Cell viability is evaluated via MTT assay. Cells (2×103?HEK-293 cells/well and 3×103?SW-839 cells/well) in 100 μL medium are seeded into 96-well plates, and incubated for 12 h. Next, the medium in each well is replaced with medium containing various concentrations of Chelerythrine Chloride, and the cells are incubated at 37°C for an additional 24 and 48 h. Subsequently, 20 μL MTT (5 mg/mL) is added to each well. Following an additional incubation at 37°C for 4 h, the supernatant is removed, and 100 μL DMSO is added to each well. The absorbance values (read at 540 nm) are determined using the iMark? Microplate Absorbance Reader. The data are analyzed using Microplate Manager software (ver. 6.3; 1689520).