Effects of silencing and overexpression of CBX8 on proliferation and apoptosis of human glioma cells / 中国病理生理杂志

AIM: To explore the effects of chromodomain protein 8 (CBX8) on the proliferation and apoptosis of human glioma cells.METHODS: The expression of CBX8 in the tissues and cells was detected by Western blot and RT-qPCR.The overexpression (Flag-CBX8) and silencing (sh-CBX8) vectors of CBX8 were constructed and transfected into glioma T98G cells and U87MG cells.The cell proliferation was detected by MTT assay and BrdU staining.The cell apoptosis was analyzed by flow cytometry.The protein expression of Rb/E2F1 was detected by Western blot.RESULTS: Compared with normal brain tissues and astrocytes, the expression of CBX8 was increased in the glioma tissues and glioma cells.Overexpression of CBX8 promoted the cell proliferation, inhibited the cell apoptosis, and upregulated the protein levels of Rb/E2F1.On the contrary, silencing of CBX8 inhibited the cell proliferation, promoted the cell apoptosis, and decreased the protein levels of Rb/E2F1 in the T98G cells and U87MG cells.Moreover, the expression of cyclin D1 and Bcl-2/Bax ratio were reduced after transfection with sh-E2F1 in the T98G cells and U87MG cells.CONCLUSION: CBX8 may regulate the proliferation and apoptosis of glioma cells through Rb/E2F1 pathway.

Mollugin inhibits viability and collagen synthesis of rat CFSC-2G cells / 中国病理生理杂志

AIM: To investigate the effects of mollugin on the viability and collagen synthesis of rat hepatic stellate cell line CFSC-2G.METHODS:The activation of CFSC-2G cells was induced with low concentration (10 μmol/L) of hydrogen peroxide (H2O2) for 30 min in the experiment.The viability of the CFSC-2G cells after exposed to mollu-gin at different concentrations (0, 20, 40, 60 and 120 μmol/L) was detected by MTT assay.The mRNA and protein ex-pression levels of nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), nuclear factor-κB (NF-κB) p65, Bcl-2, Bcl-xL, Bax, and hepatic stellate cell activation markers α-smooth muscle actin (α-SMA) and collagen type I ( ColⅠ) were detected by real-time PCR and Western blot .The phosphorylation level of p 38 mitogen-activated protein kinase ( p38 MAPK) was determined by Western blot .RESULTS:Mollugin significantly inhibited the viability and collagen syn-thesis of activated CSFC-2G cells induced by H 2 O2 .The expression of Nrf2, HO-1 and Bax at mRNA and protein levels , and the phosphorylation level of p38 MAPK were promoted, while the levels of NF-κB p65, Bcl-2, Bcl-xL, α-SMA and ColⅠwere inhibited by mollugin (P<0.05).CONCLUSION:Mollugin may inhibit H2O2-induced viability and collagen synthesis of the CSFC-2G cells by activating Nrf2 and HO-1, and blocking the NF-κB p65 and Bcl-2 expression.

Asiatic acid induces apoptosis in T98 G human glioblastoma cells by changing autophagy / 中国药理学通报

Aim To investigate the effect of asiatic acid on apoptosis and autophagy in human glioblastoma T98G cells. Methods MTT colorimetry was employed to assay the cellular proliferating activity. The fluores-cence microscope and Hoechst 33258 staining were used to detect the morphological changes. The cell ap-optosis and autophagy were analyzed by flow cytometry with Annexin-V/7-AAD and MDC staining respective-ly. The expressions of associated proteins were detected by Western blot to analyze the mechanism of apoptosis and autophagy. Results MTT assay showed that the growth of T 9 8 G cells was inhibited by asiatic acid ( IC50 =46. 3 μmol · L-1 ) . Annexin V/7-AAD stai-ning and Western blot revealed that asiatic acid in-duced apoptosis in T98 G cells by reducing the expres-sion of Akt, decreasing the mitochondrial membrane potential, and increasing the expression of Caspase-3. MDC staining and Western blot showed that the per-centage of MDC-positive cells was decreased and the expressions of Beclin-1 , LC3-II and Atgs were inhibi-ted by asiatic acid treatment. 5 μmol·L-1 chloroquine was used to up-regulate the expressions of LC3-Ⅱand Beclin-1 . Asiatic acid-inhibited autophagy was blocked and the total apoptotic rate was reduced remarkably. Conclusion Asiatic acid suppresses T98 G cells pro-liferation by inducing apoptosis and inhibiting cell au-tophagy, and the very role of inhibiting autophagy could promote apoptosis to a certain extent.

The Change of Serum Gastrin and G-cell in Gastric Antrum in Rat Model of Spleen-Qi Deficiency and the Curative Effect of Huangqi Jianzhong Decoction / 浙江中医药大学学报

[Objective]To explore the change of serum gastrin and G-cell in gastric antrum in rat model of spleen-qi deficiency and the curative effect of huangqi jianzhong decoction(HQJZD).[Methods]Spleen-qi deficiency syndrome was induced in rats by compound methods.After the models had been established,they were treated by different dosages of HQJZD.And at different time points,serum xylose,creatine phosphokinase,gastrin and G cells were observed.[Results]These indexes in groups of different dosages of HQJZD recovered gradually.Especially after 21 days' treatment,in groups of the middle and the high dosages,these indexes were increasing significantly when compared with those in the model control group(P

Effect of Helicobacter pylori infection on antral gastrin and somatostatin cells and on serum gastrin concentrations

OBJECTIVES: Helicobacter pylori infection induces selective reduction of the number of antral D-cells and results in abnormal regulation of serum gastrin secretion. The purpose of this study was to investigate the relationship between H. pylori infection and the numbers of G-cells and D-cells. METHODS: The numbers of antral G-cells and D-cells, the ratio of G-cells to D-cells and fasting serum gastrin concentrations were compared between 37 patients with (29 with duodenal ulcers and 8 with gastric ulcers) and 33 without H. pylori infection (22 with duodenal ulcers and 11 with gastric ulcers). Serum gastrin concentrations were measured using the radioimmunoassay technique. Antral mucosal biopsy specimens were examined using immunohistochemical staining with antibodies specific for gastrin and somatostatin and the numbers of G-cells and D-cells per gastric gland were counted. RESULTS: Fasting serum gastrin concentrations were significantly higher in patients with H. pylori infection compared to patients without infection (80.3 +/- 23.5 vs 47.6 +/- 14.1 pg/ml, p 0.5). The number of D-cells was significantly lower in patients with H. pylori infection than in uninfected patients in both duodenal and gastric ulcer patients (1.3 +/- 0.4 vs 2.5 +/- 1.6, respectively, p < 0.001). The ratio of G-cells to D-cells was also significantly higher in infected patients compared with uninfected patients for both gastric and duodenal ulcers (5.7 +/- 2.7 vs 3.5 +/- 1.9, respectively, p < 0.001). CONCLUSIONS: These results strongly suggest that Helicobacter pylori infection induces reduction of the number of antral D-cells. The resulting relative hypofunction of the inhibitory action of D-cells against G-cells may be responsible for increased serum gastrin secretion.

IMMUNOHISTOCHEMICAL STUDY OF D- AND G-CELLS IN THE ANTRAL MUCOSA OF THE RATS DURING SUPERIOR MESENTERIC ARTERY OCCLUSION (SMAO) SHOCK / 解剖学报

0.05)in D-and G-cells counts and G/D cell ratio between the operation and the normal control groups. But, in the shock group at 30 and 90 minutes, D-cell count was 27.9％ (P