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OBJECTIVE: To observe the effects of kaempferol (KMP) on inflammatory response and cardiomyocyte apoptosis in rats with myocardial infarction (MI), and to explore its mechanism. METHODS: Fifty rats were randomly divided into the Sham operation group (Sham), model group (MI), KMP group (received KMP), DPQ group [received poly ADP-ribose polymerase-1 (PARP-1) inhibitor] and KMP + DPQ group [received KMP combined with PARP-1 inhibitor], with 10 rats in each group. Except for the Sham group, MI models were established by ligation of left anterior descending coronary artery in other groups. After the corresponding drug treatment, the cardiac function indexes of rats were examined by echocardiography, and the activities of serum creatine kinase isoenzyme (CK-MB), cardiac troponin I (cTnI) and tumor necrosis factor-α(TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) were detected by enzyme-linked immunosorbent assay, the pathological morphology of rat myocardium was observed by hemotoxylin and eosin staining, the apoptosis of rat cardiomyocytes was detected by TUNEL staining, and the levels of TNF-α, IL-6 and IL-1β protein and PARP-1 protein expression in myocardium was detected by Western blotting. RESULTS: Compared with MI group, left ventricular end-systolic diameter and left ventricular end-diastolic diameter in the KMP group and DPQ group decreased significantly, left ventricular fractional shortening, left ventricular ejection fraction and serum CK-MB and cTnI levels increased significantly, and the pathological damage of myocardial tissue was significantly alleviated, the apoptosis rate, the levels of inflammatory factors (TNF-α, IL-6 and IL-1β) decreased significantly, and the expression of inflammatory factor-related proteins and PARP-1 protein in myocardial tissue were significantly down-regulated, with statistically significant differences (P<0. 05). The improvement of cardiac function in the KMP+DPQ group was significantly better than that in the KMP group and DPQ group (P<0. 05). CONCLUSIONS: KMP may inhibit MI and cardiomyocyte apoptosis by down-regulating PARP-1 expression, thereby improving cardiac dysfunction in rats with MI. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To probe into the effects of walnut green husk extract on proliferation, apoptosis and epidermal growth factor receptor (EGFR) / mitogen activated protein kinase (MAPK) signaling pathway of breast cancer MCF-7 cells. METHODS: Cell counting kit-8 (CCK-8) was used to screen the proper concentration of walnut husk extract interfering with breast cancer MCF-7 cells. The breast cancer MCF-7 cells were divided into the blank control group, positive control group, walnut husk husk extract low concentration group, walnut green husk extract high concentration group, walnut green husk extract high concentration + EGFR agonist (NSC228155) group. CCK-8 and colony formation experiment were used to detect cell proliferation in each group. TUNEL method and flow cytometry were used to detect cell apoptosis in each group. Western blot was used to detect the expression levels of proliferation, apoptosis and EGFR/ MAPK signaling pathway related proteins of cells in each group. RESULTS: When the concentration of walnut green husk extract was ≥20 μg/ mL, the cell proliferation rate decreased significantly, 20 μg/ mL and 40 μg/ mL were selected as the walnut green husk extract low and high concentration treatment, respectively. Compared with the blank control group, the cell proliferation rate, the number of cell colonies, the expression levels of CyclinD1, proliferating cell nuclear antigen (PCNA) and B cell lymphoma-2 (Bcl-2) protein, the ratio of phosphorylated-EGFR (p-EGFR) / EGFR, phosphorylated extracellular signal-regulated kinase (p-ERK) / extracellular signal-regulated kinase ( ERK ), phosphorylated-p38 MAPK ( p-p38 MAPK ) / p38 MAPK and phosphorylated c-Jun amino-terminal protein kinase (p-JNK) / c-Jun amino-terminal protein kinase (JNK) protein in the positive control group, the walnut green husk extract low concentration group and high concentration group decreased significantly, and the rate of TUNEL positive cells, the apoptosis rate, the expression level of Bcl-2 related X protein (Bax) increased significantly, with statistically significant differences (P<0. 05). Compared with the walnut green husk extract low concentration group, the cell proliferation rate, the number of cell colonies, the expression levels of CyclinD1, PCNA and Bcl-2 protein, the ratio of p-EGFR/ EGFR, p-ERK/ ERK, p-p38 MAPK/ p38 MAPK and p-JNK/ JNK protein in the walnut green husk extract high concentration group decreased, and the rate of TUNEL positive cells, the apoptosis rate, the expression level of Bax protein increased, with statistically significant differences (P<0. 05). There was no significant difference in the above indicators between the walnut green husk extract high concentration group and the positive control group (P >0. 05). Compared with the walnut green husk extract high concentration group, the cell proliferation rate, the number of cell colonies, the expression levels of CyclinD1, PCNA and Bcl-2 protein, the ratio of p-EGFR/ EGFR, p-ERK/ ERK, p-p38 MAPK/ p38 MAPK and p-JNK/ JNK protein in the walnut green husk extract high concentration + NSC228155 group increased, and the rate of TUNEL positive cells, the apoptosis rate, the expression level of Bax protein decreased, with statistically significant differences (P<0. 05). CONCLUSIONS: Walnut green husk extract may inhibit the proliferation of breast cancer MCF-7 cells and induce the apoptosis by inhibiting the EGFR/ MAPK signaling pathway. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To probe into the effects of ropivacaine on the proliferation, apoptosis, invasion, migration and the Ras homolog gene family member A(RhoA) / Rho-associated coiled-coil protein kinase 1(ROCK1) signaling pathway in glioma U251 cells. METHODS: Glioma U251 cells were divided into negative control group, positive control group, and ropivacaine low, medium and high dose groups. The negative control group was cultured normally without treatment, the positive control group was given 10 μg / L of cis-platinum, the ropivacaine low, medium and high dose groups were respectively given 25 mg / L, 50 mg / L and 100 mg / L of ropivacaine. After 48 h of culture, the cell proliferation rate, apoptosis rate, cell invasion number and migration distance were detected by tetramethylthiazole blue method, flow cytometry, Transwell and scratch method, the expression of RhoA, ROCK1 and matrix metalloproteinase 2 (MMP-2) protein were detected by Western blotting. RESULTS: Compared with the negative control group, the proliferation rate was decreased, the invasion number decreased, the migration distance was shortened, the expression of RhoA, ROCK1 and MMP-2 protein decreased, the apoptosis rate increased in the positive control and each dose group of ropivacain, with statistically significant differences(P<0. 05), and the ropivacaine was dose-dependent. Compared with the positive control group, the proliferation rate and the cell invasion number increased, the migration distance was prolonged, the expression of RhoA, ROCK1 and MMP-2 proteins increased, the apoptosis rate decreased in each dose group of ropivacaine, with statistically significant differences(P<0. 05). CONCLUSIONS: Ropivacaine can inhibit the proliferation, invasion and migration of glioma U251 cells, promote the apoptosis of glioma U251 cells, and the mechanism may be related to the inhibition of RhoA/ ROCK1 pathway expression. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To probe into the effects of apatinib on tumor inhibition rate and tumor cell apoptosis in breast cancer mouse model by regulating extracellular regulated kinase ( ERK) 1 / 2 pathway. METHODS: Human breast cancer cell line MCF-7 cells were inoculated in the right chest wall of nude mice, which were randomly divided into control group, low-dose group[10 mg / (kg·d) of Apatinib] and high-dose group[30 mg / ( kg·d) of Apatinib] after successful modeling, with 12 mice in each group. After intragastric administration once a day for 21 days, the tumor growth curves of three groups were plotted and the tumor inhibition rates were compared. After the last administration, the mice were executed and the tumor tissues were collected, the expression of ERK1 / 2 pathwayrelated proteins [ERK1 / 2, phosphorylated ERK1 / 2(p-ERK1 / 2)] in the tumor tissues was detected by Western blot. The effects of apatinib on MCF-7 cell cycle distribution and cell apoptosis were detected by flow cytometry. RESULTS: After processing with different concentrations of apatinib, the differences in apoptosis rate and the proportion of MCF-7 cells distributed in G0 -G1 phase were statistically significant ( P < 0. 05), among which the apoptosis rate and the proportion of MCF-7 cells distributed in G0 -G1 phase were significantly higher in the group given 20 μmol / L of apatinib than in the other low concentration groups, with statistically significant differences (P<0. 05). The tumor volumes of mice in the high-dose and low-dose groups were significantly lower than that of the control group at the 6th to 21st day of administration, with statistically significant differences (P<0. 05), of which the tumor volumes of mice in the highdose group were the smallest. The mean tumor weights of the high-dose group and low-dose group on the 22nd day were respectively (0. 343±0. 089) g and (0. 658±0. 145) g, which were significantly lower than that of the control group[(1. 163±0. 231) g], with statistically significant differences(P<0. 05). The tumor inhibition rates of the highdose group and low-dose group were respectively 64. 46% and 34. 07%, and there was a dose dependence. The expression levels of ERK1 / 2 and p-ERK1 / 2 in mice in the high-dose group and low-dose group were significantly lower than those in the control group, with statistically significant difference (P<0. 05), of which the expression levels of ERK1 / 2 and p-ERK1 / 2 in mice in the high-dose group were the lowest. CONCLUSIONS: Apatinib can effectively inhibit the ERK1 / 2 signaling pathway in breast cancer cell, induce apoptosis and proliferation of tumor cells, and thus inhibit the growth of tumors in breast cancer mice. [ABSTRACT FROM AUTHOR]