Study on the relationship between SLCO1B1 and ApoE gene polymorphisms and the risk of coronary heart disease in the Mongolian population.

Objective This study aimed to analyze the influence of SLCO1B1 and APOE gene polymorphisms on coronary heart disease in Mongolian population who living in Ordos area. Methods From January 2019 to June 2020, 200 Mongolian patients with coronary heart disease admitted to our hospital and other banner hospitals were selected as the case group. At the same time, 150 randomly selected healthy Mongolian people from medical examination centers comprised the control group. The polymorphisms of SLCO1B1 (388A>G, 521 T > C) and ApoE (388 T > C, 526 C > t) were detected by real-time polymerase chain reaction. Combined with environmental data, the effect of gene polymorphism on coronary heart disease was explored. Results Both SLCO1B1 and ApoE polymorphisms satisfied Hardy-Weinberg equilibrium. The SLCO1B1 genotype *1a/*1b showed the highest frequency in the case group, accounting for 35.0%, while The SLCO1B1 genotype *1b/*1b showed the highest frequency in the control group, accounting for 32.0%. Allele *1b was the most commonly seen allele in both the case group and control group (57.8% and 53.7%, respectively). Meanwhile, The difference in the distribution of SLCO1B1 *1a/*15 genotype between the two groups was statistically significant (P < .05). Conclusion The results showed that the SLCO1B *1a/*15 genotype, ApoE ε3 /ε3 genotype, and ε3 allele reduced the risk of coronary disease in the Mongolian population, making them protective genes against this disease, while the ApoE ε4 allele increased the risk of coronary disease, making it a coronary disease risk factor.

Treatment with hydrogen molecules prevents RANKL-induced osteoclast differentiation associated with inhibition of ROS formation and inactivation of MAPK, AKT and NF-kappa B pathways in murine RAW264.7 cells.

The bone protective effects of the hydrogen molecule (H2) have been demonstrated in several osteoporosis models while the underlying molecular mechanism has remained unclear. Osteoclast differentiation is an important factor related to the pathogenesis of bone-loss related diseases. In this work, we evaluated the effects of incubation with H2 on receptor activator of NFκB ligand (RANKL)-induced osteoclast differentiation. We found that treatment with H2 prevented RANKL-induced osteoclast differentiation in RAW264.7 cells and BMMs. Treatment with H2 inhibits the ability to form resorption pits of BMMs stimulated by RANKL. Treatment with H2 reduced mRNA levels of osteoclast-specific markers including tartrate resistant acid phosphatase, calcitonin receptor, cathepsin K, metalloproteinase-9, carbonic anhydrase typeII, and vacuolar-type H(+)-ATPase. Treatment with H2 decreased intracellular reactive oxygen species (ROS) formation, suppressed NADPH oxidase activity, down-regulated Rac1 activity and Nox1 expression, reduced mitochondrial ROS formation, and enhanced nuclear factor E2-related factor 2 nuclear translocation and heme oxygenase-1 activity. In addition, treatment with H2 suppressed RANKL-induced expression of nuclear factor of activated T cells c1 and c-Fos. Furthermore, treatment with H2 suppressed NF-κB activation and reduced phosphorylation of p38, extracellular signal-regulated kinase, c-Jun-N-terminal kinase, and protein kinases B (AKT) stimulated with RANKL. In conclusion, hydrogen molecules prevented RANKL-induced osteoclast differentiation associated with inhibition of reactive oxygen species formation and inactivation of NF-κB, mitogen-activated protein kinase and AKT pathways.

[Sanggenon C induces apoptosis of prostate cancer PC3 cells by activating caspase 3 and caspase 9 pathways].

OBJECTIVE: To investigate the effects of Sanggenon C in inducing apoptosis of prostate cancer PC3 cell line and explore the underlying mechanism. METHODS: The proliferation of PC3 cells treated for 24 h with 1, 5, 20, 50, and 100 µmol/L sanggenon C or treated with 20 µmol/L Sanggenon C for 0, 6, 12, 24 and 48 h was evaluated using MTT assay. Flow cytometry was performed for analysis of apoptosis of PC3 cells after exposure to sanggenon C with different treatment protocols, and the activity of caspase 3 was detected using spectrofluorometry. The inhibitory effect of sanggenon C on PC3 cells pretreated with DMSO, z-DEVD-fmk, z-LEHD-fmk or z-IETD-fmk for 1 h was detected by MTT assay. RESULTS: Sanggenon C inhibited the proliferation of PC3 cells in a dose- and time-dependent manner (P<0.05 except for 1 µmol/L group) with a 24-h IC50 of 18.76 µmol/L. Sanggenon C at 20 µmol/L caused inhibition rates of PC3 cells of 10.57%, 27.09%, 51.88%, 80.73% and 87.99% after treatment for 6, 12, 24, 48, and 72 h, respectively (P<0.05), and resulted in apoptosis rates of 7.43%, 20.91% and 37.56% at 12 h, 24 h and 48 h, respectively. Sanggenon C significantly increased caspase-3 activity in the cells, and its effect on PC3 cell proliferation was partially reversed by caspase 3 and caspase 9 inhibitors. CONCLUSION: Sanggenon C can dose-dependently induce growth inhibition and apoptosis of PC3 cells possibly by activating caspase 9 and caspase 3 pathways.

[Experimental study on effect of gastrodia in inducing the differentiation of mesenchymal stem cells into neuron-like cells].

OBJECTIVE: To investigate the effect of gastrodia in extracorporeal oriented inducing the differentiation of mesenchymal stem cells into neuron-like cells. METHODS: Mesenchymal stem cells were separated from bone marrow of rats by wall sticking method, amplifying cultured in vitro, and differentiated into neuron-like cells by oriented induction with gastrodia. The morphology of cells was observed under light microscopy, neuro-specific enolase (NSE), nestin and glial fibrillary acidic protein (GFAP) were detected by immunocytochemistry. RESULTS: Rats mesenchymal stem cells could be separated and amplified in vitro. After being induced by gastrodia for 2 hrs, most of the cells would be differentiated into meuron-like cells, revealing cytodendrite. By immunochemical staining, cells showed positive of NSE, nestin, and negative of GFAP. CONCLUSION: Rats' mesenchymal stem cells could be induced to differentiate into neuron-like cells.