Dihydromyricetin inhibits proliferation and migration of gastric cancer cells through regulating Akt/STAT3 signaling pathways and HMGB1 expression / 南方医科大学学报

OBJECTIVE@#To investigate the inhibitory effects of dihydromyricetin on the proliferation and migration of gastric cancer BGC-823 cells and explore the molecular mechanisms.@*METHODS@#BGC-823 cells in routine culture were treated with different concentrations of dihydromyricetin (0, 40, 60, 80, 100, and 120 μg/mL) for 24 h, and the changes in cell viability were detected using CCK-8 assay; colony forming assay and Transwell assay were performed to assess the changes in colonyforming and migration abilities of the cells, respectively. The levels of MMP-2 and MMP-9 in the treated cells were determined using ELISA, and Western blotting was used to detect the expressions of E-cadherin, N-cadherin, cyclin D1, cyclin E1, HSP70 and HMGB1 and the phosphorylation levels of Akt and Stat3.@*RESULTS@#CCK-8 assay showed that dihydromyricetin treatment dose-dependently inhibited the viability of BGC-823 cells (@*CONCLUSIONS@#Dihydromyricetin inhibits the proliferation and migration of BGC-823 cells through suppressing the activation of Akt/stat3 signaling pathways and HMGB1 expression.

Calenduloside E inhibits lipopolysaccharide-induced inflammatory response by inhibiting activation of ROS-mediated JAK1-stat3 signaling pathway in RAW264.7 cells / 南方医科大学学报

OBJECTIVE@#To investigate the effect of calenduloside E on lipopolysaccharide (LPS)-induced inflammatory response in RAW264.7 cells and explore the underlying molecular mechanism.@*METHODS@#CCK-8 assay was used to examine the effect of different concentrations of calenduloside E (0-30 μg/mL) on the viability of RAW264.7 cells. The release of the pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in RAW264.7 cells in response to pretreatment with 6, 8, and 10 μg/mL calenduloside E for 2 h followed by stimulation with 100 ng/mL LPS was detected using enzyme-linked immunosorbent assay (ELISA). The expression levels of iNOS and COX-2 and the activation of JAK-stats, MAPKs and NF-кB signaling pathways in the treated cells were determined using Western blotting. A reactive oxygen species (ROS) detection kit was used to detect ROS production in the cells, and the nuclear translocation of the transcription factor stat3 was observed by laser confocal microscopy.@*RESULTS@#Calenduloside E below 20 μg/mL did not significantly affect the viability of RAW264.7 cells. Calenduloside E dose-dependently decreased the expression levels of iNOS and COX-2 induced by LPS, inhibited LPS-induced release of TNF-α and IL-1β, and suppressed LPS-induced JAK1-stat3 signaling pathway activation and stat3 nuclear translocation. Calenduloside E also significantly reduced ROS production induced by LPS in RAW264.7 cells.@*CONCLUSIONS@#Calenduloside E inhibits LPS-induced inflammatory response by blocking ROS-mediated activation of JAK1-stat3 signaling pathway in RAW264.7 cells.

Aloin induces apoptosis regulating the activation of MAPKs signaling pathway in human gastric cancer cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of aloin on apoptosis of human gastric cancer cells and explore the molecular mechanism.</p><p><b>METHODS</b>Gastric cancer MKN-28 and HGC-27 cells were cultured routinely in 1640 medium supplemented with 10% fetal bovine serum and 10% non-essential amino acids (for HGC-27 cells) and treated with different concentrations of aloin for different durations. The cell viability, cell nuclear morphology, and apoptotic rate of the cells were detected using CCK-8 assay, DAPI staining and AnnexinV-FITC/PI, respectively; Western blotting was used to detect the expression levels of PARP, procaspase 3 and the phosphorylation of p38, ERK and JNK. The cells were treated with specific inhibitors of p38, ERK and JNK, and the inhibitory effects on these pathways were detected with Western blotting; DAPI staining was used to detect the effects of inhibitors on apoptosis of gastric cancer cells.</p><p><b>RESULTS</b>Aloin dose-dependently inhibited the viability and induced apoptosis of HGC-27 and MKN-28 cells. Alion treatment obvious enhanced the phosphorylation of p38 and JNK but decreased ERK phosphorylation in the cells. Blocking ERK activation with the ERK inhibitor obviously enhanced aloin-induced cell apoptosis, where inhibiting p38 and JNK activation partly reversed alion-induced apoptosis in the cells.</p><p><b>CONCLUSIONS</b>Aloin induces apoptosis of human gastric cancer cells by activating p38 and JNK signaling pathways and inhibiting ERK signaling pathway.</p>

Chrysin promotes SMMC-7721 cell apoptosis by regulating MAPKs signaling pathway / 南方医科大学学报

<p><b>OBJECTIVE</b>To study the effect of chrysin in inducing apoptosis of human hepatic carcinoma cells and explore the possible mechanism.</p><p><b>METHODS</b>Human hepatic carcinoma SMMC-7721 cells treated with DMSO or chrysin at different concentrations (5-200 μg/mL) were examined for changes in the cell proliferation using CCK-8 assay. The morphological changes of SMMC-7721 cells were observed in response to treatment with 5, 10, or 20 μg/mL chrysin, and the changes in the cell nuclei were observed using DAPI nuclear staining. Annexin Ⅴ-FITC/PI flow cytometry was used to determine the cell apoptosis rate. The changes in the apoptosis-related proteins (PARP and caspase-3) and MAPKs signal pathway were detected with Western blotting.</p><p><b>RESULTS</b>Chrysin treatment obviously suppressed the proliferation of SMMC-7721 cells in a dose-dependent manner below the concentration of 60 μg/mL. Chrysin (20 μg/mL) also caused significantly increased cell apoptosis and significant cleavage of PARP and caspase-3. Chrysin significantly activated MAPKs signaling pathway in a time-and dose-dependent manner, with the peak activation level occurring at 15 min. Pretreatment of the cells with specific inhibitors of the MAPKs pathway obviously inhibited the effect of chrysin in inducing cell apoptosis.</p><p><b>CONCLUSIONS</b>Chrysin inhibits the proliferation and promotes apoptosis of SMMC-7721 cells by regulating the activation of MAPKs signaling.</p>

Dual role of daphnetin in suppressing HMGB1 release and HMGB1-induced inflammation in murine macrophage RAW264.7 cells and human monocytic THP-1 cells in vitro / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the dual role of daphnetin in suppressing high mobility group box-1 protein (HMGB1) release and blocking HMGB1-induced inflammatory response.</p><p><b>METHODS</b>Murine macrophage RAW264.7 cells were cultured in the presence of daphnetin, lipopolysaccharide (LPS), or both. HMGB1 release from the cells was determined using ELISA, and phosphorylations of JAK1/2 and of STAT1 were detected by Western blotting. Human monocytic THP-1 cells exposed to daphnetin, rhHMGB1, or both were examined for NO production using a NO detection kit, for the release of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and prostaglandin E2 (PGE2) using ELISA, and for expressions of iNOS, COX-2 and phosphorylated p38, ERK, and JNK with Western blotting.</p><p><b>RESULTS</b>Daphnetin dose-dependently reduced the release of HMGB1 in RAW264.7 cells and suppressed rhHMGB1-induced iNOS and COX-2 expressions and release of TNF-α, IL-6, PGE2, and NO in THP-1 cells. Western blotting revealed that daphnetin significantly down-regulated the phosphorylations of JAK-STAT1 pathway in LPS-stimulated RAW264.7 cells but did not suppress the phosphorylations of MAPKs signaling pathway induced by rhHMGB1 in THP-1 cells.</p><p><b>CONCLUSION</b>Daphnetin can reduce the release of HMGB1 and suppress HMGB1-induced inflammatory response. In RAW264.7 cells, daphnetin inhibited LPS induced HMGB1 release is at least partly mediated by suppressing JAK-STAT1 signaling pathway activation.</p>

Study on effect of β-Sodium aescinate on vascular endothelial function, homocysteine, hypersensitive C-reactive protein and clinical efficacy in patients with acute cerebral infarction / 中国生化药物杂志

Objective To explore β-sodium aescinate on vascular endothelial function ( FMD ) , homocysteine ( Hcy ) and hypersensitive C-reactive protein ( hs-CRP) and clinical efficacy in patients with acute cerebral infarction.Methods 198 acute cerebral infarction patients from March 2013 to April 2015 were randomly divided into observation group (n=100) and control group (n=98).Control group were treated according to the condition of the disease, observation group were treated by β-sodium aescinate base on control group, 20mg was added to 250mL saline for intravenous drip,one times per day.Continuous used 14d for one treatment courses.Compared the change of vascular endothelial function, Hcy and hs-CRP and clinical efficacy.Results The total effective rate of observation group was 90.00%, which was significantly higher than that of 71.42% in control group (χ2 =11.01,P<0.05).Post-treatment the value of FMD significantly increased, Hcy and hs CRP were significantly decreased both in observation group and control group respectively, which the difference had a statistically significant as compared with Pre-treatment (P<0.05);but, the value of FMD was significantly higher, Hcy and hs CRP was significantly lower in observation group than that of control group (P<0.05).Conclusion It has a significant β-sodium aescinate clinical effect in treatment of acute cerebral infarction, and FMD are significantly higher, Hcy and hs-CRP are significantly decrease.

Effects of antisense oligonucleotide targeting survivin on apoptosis in HL-60 cells / 中国临床药理学与治疗学

AIM : To explore the effects of ASODN targeting survivin on apoptosis in HL 60 cells. METHODS : The cell proliferation was tested by MTT assay, the cell morphological transformation was observed by inverted microscope, the cell apoptosis index was examined by TUNEL, the cell apoptosis rate was precisely detected by flow cytometry, and the expression of survivin mRNA was detected by reverse transcriptase PCR. RESULTS : 5-20 ?mol?L -1 of survivin ASODN showed obviously inhibitory effect on the cell proliferation of HL 60 cells, and the inhibitory effect correlated with time and dosage. The cell apoptosis rate and the expression inhibitory rate of survivin gene in ASODN groups were obviously higher than that in the control group. Effects of antisense oligonucleotide targeting survivin on apoptosis in HL 60 cells$$$$ QI Shi mei, BI Fu yong Department of Biochemistry, Wannan Medical College, Wuhu 241001, Anhui, China ABSTRACT AIM : To explore the effects of ASODN targeting survivin on apoptosis in HL 60 cells. METHODS : The cell proliferation was tested by MTT assay, the cell morphological transformation was observed by inverted microscope, the cell apoptosis index was examined by TUNEL, the cell apoptosis rate was precisely detected by flow cytometry, and the expression of survivin mRNA was detected by reverse transcriptase PCR. RESULTS : 5-20 ?mol?L -1 of survivin ASODN showed obviously inhibitory effect on the cell proliferation of HL 60 cells, and the inhibitory effect correlated with time and dosage. The cell apoptosis rate and the expression inhibitory rate of survivin gene in ASODN groups were obviously higher than that in the control group. [WTHZ CONCLUSION : ASODN targeting survivin can effectively inhibit the expression of survivin mRNA and induce the cell apoptosis, and it indicates that survivin plays an important role in maintaining the proliferation of tumor cells.