This study aimed to explore the effects of
galangin on energy metabolism and autophagy in
gastric cancer MGC803 cells and the underlying mechanism. Cell counting kit-8(CCK-8) was used to detect the effects of
galangin at different concentrations on via-bility of MGC803 cells after 48 h intervention. Western blot was carried out to measure the effects of
galangin on expression of
proteins related to autophagy, nuclear factor-κB(NF-κB) pathway and energy metabolism, followed by the determination of its effects on
mRNA expression of energy metabolism-related
proteins by Real-time quantitative PCR(qPCR). The impact of
galangin on autophagy was explored using AutophagyGreen
dye reagent, with autophagosomes and lysosomes observed under the transmission electron microscope(TEM). Nude mice transplanted with
gastric cancer MGC803 cells via
subcutaneous injection were randomly divided into the following three groups: control(0.5%
sodium carboxymethyl cellulose, once a day),
5-fluorouracil(5-FU, 50 mg·kg~(-1), twice a week), and
galangin(120 mg·kg~(-1), once a day) groups. The
body weight and
tumor volume were measured once every three days with a vernier caliper at the same time point by the same person. After 21-d treatment, the
tumor tissue was isolated and weighed for the calculation of the
tumor-suppressing rate. The comparison with the control group revealed that
galangin inhibited the viability of MGC803 cells, up-regulated the
protein expression of microtuble-associated
protein 1 light chain 3 B(LC3 B) Ⅱ, inhibited the phosphorylation of NF-κB pathway-related
proteins, and promoted the formation of autophagosomes in MGC803 cells. However, it did not obviously affect the expression of energy metabolism-related
proteins. Furthermore,
galangin at 120 mg·kg~(-1) significantly reduced the
tumor weight and volume in mice, enhanced LC3 BⅡ
protein expression, and inhibited the phosphorylation of NF-κB pathway-related
proteins. All these have suggested that
galangin inhibited the growth of
gastric cancer MGC803 cells both in vivo and in vitro, possibly by inhibiting the NF-κB pathway and enhancing autophagy.