Potentilla anserina polysaccharide alleviates cadmium-induced oxidative stress and apoptosis of H9c2 cells by regulating the MG53-mediated RISK pathway / 中国天然药物

Oxidative stress plays a crucial role in cadmium (Cd)-induced myocardial injury. Mitsugumin 53 (MG53) and its mediated reperfusion injury salvage kinase (RISK) pathway have been demonstrated to be closely related to myocardial oxidative damage. Potentilla anserina L. polysaccharide (PAP) is a polysaccharide with antioxidant capacity, which exerts protective effect on Cd-induced damage. However, it remains unknown whether PAP can prevent and treat Cd-induced cardiomyocyte damages. The present study was desgined to explore the effect of PAP on Cd-induced damage in H9c2 cells based on MG53 and the mediated RISK pathway. For in vitro evaluation, cell viability and apoptosis rate were analyzed by CCK-8 assay and flow cytometry, respectively. Furthermore, oxidative stress was assessed by 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) staining and using superoxide dismutase (SOD), catalase (CAT), and glutathione/oxidized glutathione (GSH/GSSG) kits. The mitochondrial function was measured by JC-10 staining and ATP detection assay. Western blot was performed to detect the expression of proteins related to MG53, the RISK pathway, and apoptosis. The results indicated that Cd increased the levels of reactive oxygen species (ROS) in H9c2 cells. Cd decreased the activities of SOD and CAT and the ratio of GSH/GSSG, resulting in decreases in cell viability and increases in apoptosis. Interestingly, PAP reversed Cd-induced oxidative stress and cell apoptosis. Meanwhile, Cd reduced the expression of MG53 in H9c2 cells and inhibited the RISK pathway, which was mediated by decreasing the ratio of p-AktSer473/Akt, p-GSK3βSer9/GSK3β and p-ERK1/2/ERK1/2. In addition, Cd impaired mitochondrial function, which involved a reduction in ATP content and mitochondrial membrane potential (MMP), and an increase in the ratio of Bax/Bcl-2, cytoplasmic cytochrome c/mitochondrial cytochrome c, and Cleaved-Caspase 3/Pro-Caspase 3. Importantly, PAP alleviated Cd-induced MG53 reduction, activated the RISK pathway, and reduced mitochondrial damage. Interestingly, knockdown of MG53 or inhibition of the RISK pathway attenuated the protective effect of PAP in Cd-induced H9c2 cells. In sum, PAP reduces Cd-induced damage in H9c2 cells, which is mediated by increasing MG53 expression and activating the RISK pathway.

Research Progress in Pharmacological Effects and Clinical Application of Pine Pollen / 中国中医药信息杂志

Pine pollen is a kind of Chinese materia medica with the homology of medicine and food, rich in a variety of nutrients and bioactive ingredients. It has the efficacy of hemostasis by convergence and eliminating dampness and astringing sores. Research showed that pine pollen is able to protect certain organs, regulate metabolism, enhance immunity and resist antioxidation and aging. This article reviewed pine pollen related research from the aspects of main components, pharmacological effects and clinical application, in order to provide references for further study and development and utilization.

Research Progress in Extraction, Purification and Bioactivities of Potentilla Anserine Polysaccharide / 中国中医药信息杂志

As a common Tibetan medicine, Potentilla anserine L. is a kind of important Chinese materia medica, which is mainly distributed in Gansu, Qinghai and Tibet Provinces. As the active constituent from Potentilla anserine L., potentilla anserine polysaccharide has received initial research by researchers in abroad and at home. It is suggested that potentilla anserine polysaccharide exhibits various functions including antioxidation, anti-aging, immunoregulation, inhibiting bacteria and anti-diabetic. This article reviewed the research on extraction, purification and bioactivities of potentilla anserine polysaccharide, which is expected to provide ideas for the further study and research and development.

Effects of non-saccharomyces albicans metabolic products on the proliferation of human umbilical vein endothelial cell ECV304 / 华西口腔医学杂志

<p><b>OBJECTIVE</b>To evaluate the effects of non-Saccharomyces albicans metabolic products on the cell cycle distribution and proliferation of human umbilical vein endothelial cell ECV304 cells in vitro.</p><p><b>METHODS</b>The parallel dilution supernatant of Saccharomyces tropicalis, Saccharomyces krusei and Saccharomyces glabrata were prepared, and 1, 4, 16-fold(s) diluted concentration and control group were set up. The line of human umbilical vein endothelial cell ECV304 was cultured in vitro and treated by non-Saccharomyces albicans supernatant. The proliferous effect of ECV304 induced by non-Saccharomyces albicans supernatant after 24, 48, 72 h was detected by the methods of MTT, and the changes of cell density and cycle after 48 h were investigated by inverted microscope and flow cytometry.</p><p><b>RESULTS</b>At the 24th hour, all of the higher concentration (1-fold) of non-Saccharomyces albicans supernatant and the 4-folds diluted Saccharomyces krusei could promote ECV304 proliferation(P < 0.05). After adding various non-Saccharomyces albicans supernatant at 48h and 72th hour, Saccharomyces krusei supernatant and Saccharomyces glabrata supernatant significantly increased proliferation rate of ECV304, while Saccharomyces tropicalis supernatant group showed no significant change no matter which concentration was tested. At 48th hour after adding the non-Saccharomyces albicans supernatant, the ECV304 cells density treated by Saccharomyces krusei supernatant and Saccharomyces glabrata supernatant were significantly higher under the inverted microscope. The G0/G1 population of ECV304 cells decreased while cell proliferation index (PI) increased after incubated with Saccharomyces krusei supernatant and Saccharomyces glabrata supernatant for 48 hours (P < 0.05). Saccharomyces tropicalis group showed no significant change (P > 0.05).</p><p><b>CONCLUSION</b>The metabolic products of Sacharoymces krusei and Saccharomyces glabrata could induce proliferation of ECV304 cell, which suggests non-Saccharomyces albicans should be undergone more attention clinically in detection and treatment.</p>

A study on human tongue cancer cells' proliferation affected by Lactobacillus acidophilus / 华西口腔医学杂志

<p><b>OBJECTIVE</b>To study the effects of Lactobacillus acidophilus (L. acidophilus) on the proliferation and cell cycle distribution of human tongue cancer cells (Tca8113 cells).</p><p><b>METHODS</b>In vitro cultivated human Tca8113 cells were treated by L. acidophilus supernatant, inactivated bacilli, cell free extracts and normal culture medium respectively, which were 1, 4, 16-fold(s) dilutelly, to investigate the proliferous effects of Tca8113 cells using of inverted microscope, cell counting, sulforhodamine B (SRB) and flow cytometry. The free radicals and Ca2+ in Tca8113 cells were also studied by confocal laser scanning microscope (CLSM).</p><p><b>RESULTS</b>At the 48th hour after adding different L. acidophilus components, the Tca8113 cells changed in shape from the diamond-like, polygonal and slabs into the elongated form. In the condition of different times and different culture concentrations, the proliferation of Tca8113 cells was significantly inhibited by L. acidophilus components, which enhanced as the time prolonged and the concentrations of each L. acidophilus components increased according to the cell counting and the SRB experimental analysis. The cell proliferation index (CPI) was significantly reduced (P<0.01). The free radicals and Ca2+ in Tca8113 cells under the effect of each L. acidophilus components for 48 h indicated an obviously rising (P<0.01).</p><p><b>CONCLUSION</b>L. acidophilus restrains the proliferation of Tca8113 cells, which might be due to the increase in quantity of free radicals and Ca2+ in Tca8113 cells, and might be resulted from the release of metabolic products of L. acidophilus.</p>

Effects of aspirin on [Ca~(2+)] i and NGB in cultured neural cells of newborn rat under chemical-induced hypoxic exposure / 基础医学与临床

Objective To investigate the protective effects of aspirin on hypoxic brain neural cells of rat and the effects of extracellular calcium on the neuroprotective effect of aspirin. Methods The hypoxic cell model was established by adding Na_2S_2O_4 to the calcium or calcium free medium. Cultured primary cortical neurons of rat were pretreated with ASA in vitro. The change of intracellular free calcium and neuroglobin (NGB) were observed and analyzed by laser scanning confocal microscope. Results The expression level of [Ca~(2+)] i and NGB increased significantly in the chemical hypoxia group ( P < 0. 05 ). ASA can attenuate the increase of [ Ca~(2+) ] i and NGB in the hypoxic group and calcium-free hypoxia group(P <0. 05). Conclusion Aspirin can inhibit calcium overload and the hypoxia-induced expression of NGB, so protect rat brain cells against hypoxia.

Effects of aspirin on [Ca~(2+)]i and NGB in cultured neural cells of newborn rat under chemical-induced hypoxic exposure / 基础医学与临床

Objective To investigate the protective effects of aspirin on hypoxic brain neural cells of rat and the effects of extracellular calcium on the neuroprotective effect of aspirin. Methods The hypoxic cell model was established by adding Na2S2O4 to the calcium or calcium free medium. Cultured primary cortical neurons of rat were pretreated with ASA in vitro. The change of intracellular free calcium and neuroglobin (NGB) were observed and analyzed by laser scanning confocal microscope. Results The expression level of [Ca2+]i and NGB increased significantly in the chemical hypoxia group(P

Effects of fuzheng yiliu granules on apoptotic rate and mitochondrial membrane potential of hepatocellular carcinoma cell line H22 from mice / 中西医结合学报

OBJECTIVE: To evaluate the effects of Fuzheng Yiliu Granules (FZYLG) on apoptotic rate and mitochondrial membrane potential (Delta psi m) of hepatocellular carcinoma cell line H22 from mice. METHODS: Forty-eight mice inoculated with H22 cells were randomly divided into four groups: untreated group, cyclophosphamide-treated group, high-dose FZYLG-treated group and low-dose FZYLG-treated group. After 14 days of corresponding treatment, H22 cells in each group were stained with propidium iodide, and the apoptotic rates were detected by flow cytometry (FCM). The rhodamine 123 was used as a fluorescence probe to label the H22 cells, and the fluorescence intensities were observed with laser scanning confocal microscope. The fluorescence intensity of H22 cells indicated the Delta psi m of H22 cells. RESULTS: FZYLG could significantly increase the apoptotic rate while reduce the Delta psi m of H22 cells from mice as compared with those in the untreated group. CONCLUSION: The antitumor effects of FZYLR on H22 cells from mice are related to decreasing the Delta psi m and then inducing the apoptosis of the H22 cells.

Arsenic trioxide inhibits p-glycoprotein expression in multidrug-resistant human leukemia cells that overexpress the MDR1 gene / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the effects of arsenic trioxide (As(2)O(3)) on the apoptosis and p-glycoprotein (P-gp) expression of multidrug-resistant human leukemia cells.</p><p><b>METHODS</b>Human multidrug-resistant leukemia cell line K562/ADM overexpressing the MDR1 gene, was used as the target cells. The cell proliferating activity was assessed using the MTT colorimetric assay. Cytomorphology was investigated under light, confocal and electron microscopes. DNA fragmentation was examined using agarose gel electrophoresis, while p-gp expression, cell cycle status and sub-G1 cells were determined using flow cytometry.</p><p><b>RESULTS</b>Zero point five to 20 micromol/L As(2)O(3) inhibited the proliferation of K562/ADM cells, and K562/ADM cells were more sensitive to As(2)O(3) than the parental K562 cells. As(2)O(3)-induced apoptosis of K562/ADM cells was determined by the observance of typical morphological changes and the appearance of DNA ladder and sub-G1 cell populations. As(2)O(3) significantly inhibited the P-gp expression of K562/ADM cells, and synergistically enhanced the sensitivity of the drug-resistant cells to adriamycin.</p><p><b>CONCLUSIONS</b>As(2)O(3) induces growth-inhibition and apoptosis, down-regulates P-gp expression and exerts a synergistic effect in combination with adriamycin in multidrug-resistant leukemia cells.</p>