The inhibitory effects of diallyl sulfide (DAS) derived from allicin on in vitro and in vivo proliferation of human osteosarcoma MG-63 cells and the action mechanism, and the influence of DAS on invasive capability of MG-63 cells were investigated in order to search for the novel medicines for osteosarcoma. In the in vitro experiment, MG-63 cells were treated with different concentrations of DSA, and the morphological changes of MG-63 cells were observed under an inverted phase microscope. MTT method was used to assay the proliferation of MG-63 cells. Semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to detect the VEGF mRNA expression level in MG-63 cells. By using Transwell invasion assay, the influence of DAS on invasive ability of MG-63 cells was tested. In the in vivo experiment, the nude mice MG-63 cells tumor-bearing model was established, and different concentrations of DAS were injected beside the tumor. Twenty-one days after treatment, the mice were killed, the tumor size and tumor inhibition rate were calculated. The microvessel density (MVD) was determined by using immunohistochemistry. In the in vitro experiment, different concentrations of DAS could obviously inhibit proliferation of MG-63 cells in a time- and concentration-dependent manner. RT-PCR revealed that the expression levels of VEGF mRNA in DSA groups (different concentrations) were significant reduced as compared with those in control group (all P<0.05). Transwell invasion assay indicated that in 20 and 40 μg/mL DAS groups, the number of migratory cells was 91.4±8.3 and 81.8±7.4 respectively, which was significantly declined as compared with that in control group (150.4±14.7, both P<0.05). In the in vivo experiment, DAS could significantly suppress the growth of MG-63 tumor-bearing tissue. Immunohistochemistry demonstrated that different concentrations (20 and 40 μg/mL) of DAS could significantly decrease MVD of MG-63 tumor-bearing tissue (all P<0.05). It was suggested that DAS could inhibit the growth of MG-63 cells probably by suppressing the expression of VEGF mRNA.

This paper summarized researches about the factors that influenced the measurement of hand grip, including equipments, ethnics,genders, ages, morphological parameters, handedness, occupation, grip width, body posture and psychological factors. All these are to be considered in studies of grip strength.

Objective To investigate the relationship between QRS wave terminal distortion with coronary arterial lesion and serum high-sensitivity cardiac troponin I (hs-cTnI) in early stage of acute ST-segment elevation myocardial infarction (STEMI).Methods One hundred and twenty patients with STEMI were classified into the QRS wave distortion positive group(QRS+,n=81) and non-QRS wave distortion group(QRS-group,n=39) according to EKG on admission.The two groups all conducted the coronary angiography and hs-cTnI detection.The coronary arterial lesion occurrence situation and hs-cTnI level were compared between the two groups.Results (1) In the QRS+ group:68 cases (83.59％) were male and 13 cases (16.05％) were females;in the QRS-group:27 cases(69.23％) were male and 12 cases (30.77％) were female.The sex difference had statistical significance (P＜0.05).(2) The occurrence rate of left anterior descending artery (LAD) lesion in the QRS+ group was higher than that in the QRS-group,the difference was statistically significant (P＜0.05).But the occurrence rate of left circumflex coronary artery (LCX) lesion in the QRS-group was higher than that in the QRS+ group,the difference was statistically significant (P＜0.01).(3) The hs-cTnI level in the QRS+ group was higher than that in the QRS-group,the difference was statistically significant (P ＜0.01).Conclusion The patients with QRS wave distortion positive have a higher occurrence rate of LAD lesion,while the patients with out QRS wave distortion negative have higher occurrence rate of LCX lesion;the QRS wave terminal distortion has relationship with serum hs-cTnI level.

The inhibitory effects of diallyl sulfide (DAS) derived from allicin on in vitro and in vivo proliferation of human osteosarcoma MG-63 cells and the action mechanism, and the influence of DAS on invasive capability of MG-63 cells were investigated in order to search for the novel medicines for osteosarcoma. In the in vitro experiment, MG-63 cells were treated with different concentrations of DSA, and the morphological changes of MG-63 cells were observed under an inverted phase microscope. MTT method was used to assay the proliferation of MG-63 cells. Semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to detect the VEGF mRNA expression level in MG-63 cells. By using Transwell invasion assay, the influence of DAS on invasive ability of MG-63 cells was tested. In the in vivo experiment, the nude mice MG-63 cells tumor-bearing model was established, and different concentrations of DAS were injected beside the tumor. Twenty-one days after treatment, the mice were killed, the tumor size and tumor inhibition rate were calculated. The microvessel density (MVD) was determined by using immunohistochemistry. In the in vitro experiment, different concentrations of DAS could obviously inhibit proliferation of MG-63 cells in a time- and concentration-dependent manner. RT-PCR revealed that the expression levels of VEGF mRNA in DSA groups (different concentrations) were significant reduced as compared with those in control group (all P<0.05). Transwell invasion assay indicated that in 20 and 40 μg/mL DAS groups, the number of migratory cells was 91.4±8.3 and 81.8±7.4 respectively, which was significantly declined as compared with that in control group (150.4±14.7, both P<0.05). In the in vivo experiment, DAS could significantly suppress the growth of MG-63 tumor-bearing tissue. Immunohistochemistry demonstrated that different concentrations (20 and 40 μg/mL) of DAS could significantly decrease MVD of MG-63 tumor-bearing tissue (all P<0.05). It was suggested that DAS could inhibit the growth of MG-63 cells probably by suppressing the expression of VEGF mRNA.
Allyl Compounds ; pharmacology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Neoplasm Invasiveness ; prevention & control ; Osteosarcoma ; drug therapy ; Sulfides ; pharmacology

Objective This study investigated the protective effects of Corni Fructus ethanol extract on β-amyloid protein 25-35 (Aβ25-35)-induced Alzheimer's disease (AD) mice by regulating histone lysine-specific demethylase 1 (LSD1) / postsynaptic density protein 95 (PSD95) on synapses and neuroinflammation. Methods Specifically, according to the body weight, 40 C57BL/6N mice were randomized into four groups: the sham operation group, the model group, the low-dose (0.1mg/g) and the high-dose (0.3 mg/g) Corni Fructus ethanol extract groups. Aβ25-35 was injected into the hippocampus of mice in three groups except for the sham operation group to established AD model. All mice were orally administered with either Corni Fructus ethanol extract or vehicle by gavage for 7 days before molding and continued 5 days after surgery for a total of 60 days. Morris water maze, Y maze and open field tests were performed to evaluate the recognition memory and space exploration ability of mice. The expression of LSD1, PSD95, synaptophysin (SYN), interleukin-1β (IL-1β), tumor necrosis factor-α(TNF-α) and H3K9me2 level were measured by Western blotting. Chromatin immunoprecipitation (CHIP) combined with qPCR was used to detect H3K9me2 modification of PSD95 promoter region and mRNA levels of PSD95. The correlation between the expression of H3K9me2 and PSD95 and the expression of IBA1 in the hippocampus were detected by immunofluorescence assay.Results The result showed that Corni Fructus ethanol extract significantly reversed Aβ25-35-induced learning and memory impairment in AD mice. Compared with the model group, Corni Fructus ethanol extract demonstrated shorter escape latency, increased number and time of autonomous activities and the rate of autonomous alternation. Moreover, it increased the expression of LSD1 in hippocampus of AD mice(P<0.05), and reduced H3K9me2 modification level in the promoter region of PSD95 gene, and then promoted the mRNA transcription and protein expression of PSD95. Immunofluorescence staining indicated the reduction of H3K9me2 modification level in hippocampus was accompanied by the enhancement of PSD95 expression. Corni Fructus ethanol extract could also inhibit the activation of microglia and reduce the expression of proinflammatory factors IL-1β and TNF-α.Conclusion Corni Fructus ethanol extract may regulate PSD95 gene transcription by up-regulating the expression of LSD1 and reducing the H3K9me2 modification level in its promoter region, thereby increasing the expression of PSD95, a key protein in synaptic plasticity regulation, which alleviate neuroinflammatory response, improve learning and memory dysfunction in AD model mice, and thus play a protective role in Aβ25-35-induced nerve damage.