Among various Ser/Thr protein kinases, CKII plays a potential role in the processes of cell proliferation, transformation, and differentiation. In addition, abolition of CKII activity causes cell death in yeast, whereas overexpression of the CKII α-subunit gene in animal cells causes the cells to become oncogenic. Emodin, an anthraquinone derivative, selectively and competitively inhibits CKII with IC50 of 2 μM and Ki of 7.2 μM[5]. HepG2 cells treated with 25 μM emodin for 48 h displayed apoptotic morphological changes[6]. Emodin killed T24 and J82 cells in a dose-dependent manner after 24 h treatment. It also killed T24 at concentration of 20 μM and J82 cells at concentration of 15 μM in a time-dependent manner. Mice treated with emodin and cisplatin had significantly smaller tumors than those from the other groups indicating emodin/cisplatin co-treatment can significantly suppress tumor growth in vivo[7].
Emodin/大黄素 细胞实验
Cell Line
Concentration
Treated Time
Description
References
MDCK cells
25 μg/mL
48 hours
To detect the inhibitory effect of Emodin-8-glucoside on IAV replication. The results showed that Emodin-8-glucoside significantly inhibited IAV replication.
Biomed Res Int. 2021 Sep 9;2021:9066938
A549 cells
25 μg/mL
48 hours
To detect the inhibitory effect of Emodin-8-glucoside on IAV replication. The results showed that Emodin-8-glucoside significantly inhibited IAV replication.
Biomed Res Int. 2021 Sep 9;2021:9066938
Emodin/大黄素 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
BALB/c mice
IAV infection model
Oral gavage
75 mg/kg/day
Once daily from -1 to 5 days post infection
To detect the protective effect of Emodin-8-glucoside on IAV-infected mice. The results showed that Emodin-8-glucoside significantly improved the average survival time of mice, reduced lung index, lung cytokines, and pulmonary viral load.
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