DOI: 10.57760/sciencedb.j00217.03861
title: Gallic acid activates T cells through CD137 signaling and induces apoptosis in liver cancer cells
title: 没食子酸通过CD137信号激活T细胞诱导肝癌细胞凋亡

description: Objective To explore the role of gallic acid ( GA ) in inducing apoptosis of hepatocellular carcinoma cells by activating T cells through CD137 signal, and to explore its related mechanism.Methods Six-week-old C57BL / 6 and CD137- / -male mice were 15 each. After modeling, C57BL / 6 mice were randomly divided into WT mouse control group, gallic acid WT mouse treatment group, and sorafenib WT mouse treatment group. CD137- / -mice were randomly divided into KO mouse control group, gallic acid KO mouse treatment group, and sorafenib KO mouse treatment group. On the day of grouping, the gallic acid WT mice and KO mice treatment group were given gallic acid injection by gavage at 5g / kg, once a day, 0.1ml each time ; the sorafenib WT mice and KO mice treatment group were intragastrically administered with 30 mg / kg once a day, 0.2 ml / time. The control group was given equal volume of 0.9 % sodium chloride injection, once a day. Continuous administration for 2 weeks. Tunel staining analysis was used to detect apoptosis;ki67 histochemistry was used to detect cell proliferation. Immunofluorescence analysis was used to observe the number of T cells and the relationship between CD137 and T cells. Western blotting was used to detect the expression of T cell activation markers, apoptosis-related proteins, perforin and granzyme.Results Tunel staining and analysis showed that the apoptosis of liver cancer cells in GA treatment group ; ki67 histochemistry analysis showed that the proliferation ability of liver cancer cells in GA treatment group was decreased. Immunofluorescence analysis showed that the number of T cells in the GA treatment group increased, and CD137 was positively correlated with T cells. Western blotting showed that the expression of T cell activation markers, apoptosis-related proteins, perforin and granzyme were increased in the GA treatment group.Conclusion GA can inhibit the proliferation of hepatocellular carcinoma cells and induce apoptosis of cancer cells. The mechanism may be related to the activation of CD137 signaling pathway and the increase of T cell activity.
description: Objective To explore the role of gallic acid ( GA ) in inducing apoptosis of hepatocellular carcinoma cells by activating T cells through CD137 signal, and to explore its related mechanism.Methods Six-week-old C57BL / 6 and CD137- / -male mice were 15 each. After modeling, C57BL / 6 mice were randomly divided into WT mouse control group, gallic acid WT mouse treatment group, and sorafenib WT mouse treatment group. CD137- / -mice were randomly divided into KO mouse control group, gallic acid KO mouse treatment group, and sorafenib KO mouse treatment group. On the day of grouping, the gallic acid WT mice and KO mice treatment group were given gallic acid injection by gavage at 5g / kg, once a day, 0.1ml each time ; the sorafenib WT mice and KO mice treatment group were intragastrically administered with 30 mg / kg once a day, 0.2 ml / time. The control group was given equal volume of 0.9 % sodium chloride injection, once a day. Continuous administration for 2 weeks. Tunel staining analysis was used to detect apoptosis;ki67 histochemistry was used to detect cell proliferation. Immunofluorescence analysis was used to observe the number of T cells and the relationship between CD137 and T cells. Western blotting was used to detect the expression of T cell activation markers, apoptosis-related proteins, perforin and granzyme.Results Tunel staining and analysis showed that the apoptosis of liver cancer cells in GA treatment group ; ki67 histochemistry analysis showed that the proliferation ability of liver cancer cells in GA treatment group was decreased. Immunofluorescence analysis showed that the number of T cells in the GA treatment group increased, and CD137 was positively correlated with T cells. Western blotting showed that the expression of T cell activation markers, apoptosis-related proteins, perforin and granzyme were increased in the GA treatment group.Conclusion GA can inhibit the proliferation of hepatocellular carcinoma cells and induce apoptosis of cancer cells. The mechanism may be related to the activation of CD137 signaling pathway and the increase of T cell activity.