Chloroquine enhances catalpol's ability to promote apoptosis by inhibiting catalpol's autophagy-promoting effect on gastric cancer

氯喹通过抑制梓醇对胃癌的自噬促进作用增强梓醇促进细胞凋亡的能力

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作者:Fangzheng Sun, Zhenghua Wang, Xiaoyu Wang

Conclusions

In summary, the above results indicate that inhibition of catalpol-induced autophagy could better promote the apoptosis of gastric cancer cells.

Methods

In this experiment, we studied the effect of catalpol from the extract of Dihuang from traditional Chinese medicine on gastric cancer cells.

Purpose

Gastric cancer, which is derived from gastric mucosal epithelial cells, is a representative solid tumour, and more than 1 million cases are diagnosed worldwide each year. However, treatment

Results

The results showed that catalpol led to a dose-dependent reduction in gastric cancer cell proliferation. When the promotion of autophagy by catalpol was inhibited, the proapoptotic effects of catalpol on gastric cancer cells were enhanced. Bax, an apoptosis-related marker, was upregulated in catalpol-treated cells, and its expression was increased in the group treated with catalpol in combination with an inhibitor compared to the group treated with catalpol alone. Opposite results were obtained with BCL-2 inhibition. Flow cytometry showed that apoptosis rates were higher in cells treated with a combination of autophagy inhibitors. Accumulation of reactive oxygen species (ROS) in gastric cancer cells showed the group treated with the combination of catalpol and an inhibitor enhanced ROS production. Transwell assays showed that catalpol plus autophagy inhibitors exerted a stronger inhibitory effect on the migration ability of AGS cells than catalpol alone. Conclusions: In summary, the above results indicate that inhibition of catalpol-induced autophagy could better promote the apoptosis of gastric cancer cells.

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