ObjectiveTo investigate the protective effect of pinocembrin (PIN) in a mouse model of liver injury induced by acetaminophen (APAP). MethodsA total of 50 healthy male C57BL/6J mice were randomly divided into blank group, PIN (50 mg/kg) group, APAP (300 mg/kg) model group, PIN (30 mg/kg)+APAP (300 mg/kg) experimental group, and PIN (50 mg/kg)+APAP (300 mg/kg) experimental group, with 10 mice in each group. The mice in the blank group and the model group were given an equal volume of normal saline by gavage, and those in the PIN group and the PIN+APAP groups were given PIN by gavage once a day, for 7 consecutive days. At 2 hours after the last administration, the mice in the model group and the PIN+APAP groups were given intraperitoneal injection of APAP 300 mg/kg once, and those in the blank group and the PIN group were given intraperitoneal injection of an equal volume of normal saline. Serum samples were collected to measure the levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST); liver tissue homogenate was prepared to measure the biochemical parameters of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH); HE staining was used to observe liver histopathology. A one-way analysis of variance was used for comparison of continuous data between multiple groups, and the least significant difference t-test was used for further comparison between two groups. ResultsCompared with the blank group, the APAP (300 mg/kg) model group had significant increases in the activities of ALT and AST (P＜0.01), suggesting that a model was successfully established, while the PIN (30 mg/kg)+APAP (300 mg/kg) group and the PIN (50 mg/kg)+APAP (300 mg/kg) group had significant reductions in the levels of ALT and AST (P＜0.01). Compared with the blank group, the APAP (300 mg/kg) model group had a significant increase in the level of MDA and significant reductions in SOD activity and GSH level in the liver (P＜001); compared with the APAP (300 mg/kg) model group, the PIN (30 mg/kg)+APAP (300 mg/kg) group and the PIN (50 mg/kg)+APAP (300 mg/kg) group had a significant reduction in the level of MDA and significant increases in SOD activity and GSH level in the liver (P＜0.05). Histopathological observation showed that PIN significantly improved liver injury caused by APAP and helped to maintain normal liver histomorphology. ConclusionPIN exerts a marked protective effect on liver injury induced by APAP, possibly by inhibiting oxidative stress in the liver.

ObjectiveTo investigate the effect of kaempferol on the proliferation, migration, invasion, and apoptosis of human hepatoma Bel-7402 cells and related molecular mechanism. MethodsHepatoma Bel-7402 cells cultured in vitro were randomly divided into control group and low-, middle-, and high-concentration experimental groups. The experimental groups were treated with low-, middle-, and high-concentration kaempferol (25, 50, and 100 μmol/L), and the control group was treated with an equal volume of dimethyl sulfoxide. CCK-8 assay was used to observe the effect of kaempferol on the viability of Bel-7402 cells; plate colony formation assay was used to evaluate the effect of kaempferol on cell colony formation ability; wound healing assay and Transwell chamber were used to observe the effect of kaempferol on cell migration and invasion; Western blot was used to measure the expression of apoptosis- and cycle-related proteins. A one-way analysis of variance was used for comparison between multiple groups, and the least significant difference t-test was used for further comparison between two groups. ResultsAfter 24 hours of treatment, the cell viability was 100.00%±2.72% in the control group and 75.70%±2.42%, 62.79%±2.45%, and 43.41%±2.11%, respectively, in the low-, middle-, and high-concentration experimental groups, and compared with the control group, the experimental groups had a significant reduction in cell viability (all P＜0.05). The number of cell colonies was 923.3±35.2 in the control group and 682.7±24.4, 464.0±22.0, and 327.3±14.0, respectively, in the low-, middle-, and high-concentration experimental groups, and compared with the control group, the experimental groups had a significant reduction in cell colony formation ability (all P＜0.05). After 24 hours of treatment, the relative migration rate was 100.00%±1.11% in the control group and 63.33%±1.16%, 51.72%±3.23%, and 37.18%±2.71%, respectively, in the low-, middle-, and high-concentration experimental groups, and the number of transmembrane cells was 212.0±3.0 in the control group and 134.0±2.0, 71.0±2.0, and 34.0±1.0, respectively, in the low-, middle-, and high-concentration experimental groups; compared with the control group, the experimental groups had significant reductions in relative migration rate and number of transmembrane cells (all P＜0.05). After 48 hours of treatment, compared with the control group, the low-, middle-, and high-concentration experimental groups had a significant reduction in the expression of the anti-apoptotic protein Bcl-2 (all P＜0.05), a significant increase in the expression of the pro-apoptotic protein Bax (all P＜0.05), and a significant reduction in the expression of C＜italic/＞yclinD1 (all P＜005). ConclusionKaempferol can inhibit the proliferation, migration, and invasion of human hepatoma Bel-7402 cells and promote the apoptosis of such cells, possibly by regulating the apoptosis proteins Bax and Bcl-2 and downregulating the expression of CyclinD1.