ABSTRACT
Stroke is a neurological disease which is difficult to conquer clinically .Cell transplantation based on mesenchymal stem cells(MSCs) provides hope for the healthy recovery of stroke patients , but our study of MSCs for stroke therapy is not thorough enough and still faces some problems .The aim of this paper is to summarize the problems with MSCs in the treatment of stroke from the perspectives of tissue source , preparation process, time window, transplantation pathway , pretreatment , combined medication and tracer method , in order to provide guidance for scientific research and clinical application.
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Aim To investigate the effect of miR-320a up-regulation on the apoptosis and migration of Bel7402 cells induced by ribonucleic acid Ⅱ.Methods The different expression levels of miR-320a in normal liver cells and hepatocellular carcinoma (HCC) cells were detected by qRT-PCR.Bel-7402 cell was transfected with miR-320a mimic,and the miR-320a expression levels were measured by qRT-PCR.The effect of ribonucleic acid Ⅱ on proliferation of Bel-7402 and Bel-7402-miR-320a cells was measured by CCK-8 assay,and cell cycle and apoptosis were detected by flow cytometry.The migration and invasion ability of ribonucleic acid Ⅱ on Bel-7402 cells were tested by Transwell method.The expression of p53,Cyclin D1,Bax,Bcl-2,MMP-3 proteins were examined by Western blot.Results miR-320a expression levels in HCC cell line Bel-7402 were significantly lower than those in normal cell line HL-7702.Bel-7402 cells were successfully transfected with miR-320a mimic,named Bel-7402-miR-320a.CCK-8 showed that ribonucleic acid Ⅱ could effectively inhibit the proliferation of Bel7402 and Bel-7402-miR-320a cells in vitro in a dosedependent manner at the range of 100,200,300,400,500 mg · L-1.The IC50 of ribonucleic acid Ⅱexposure on Bel-7402 and Bel-7402-miR-320a cells for 12 h and 24 h was 250,200 mg · L-t and 150,120 mg · L-1,respectively;flow cytometric analysis indicated that over-expression of miR-320a could arrest Bel-7402 and Bel-7402-miR-320a cells induced by ribonucleic acid Ⅱ in G0/G1 phase,and promote the apoptosis of HCC cells.Transwell method showed that Bel-7402-miR-320a + Ribonucleic acid Ⅱ group could significantly inhibit the migration of HCC cells compared with control group and Bel-7402 + Ribonucleic acid Ⅱ group.Western blot results showed that the expression of p53,Bax proteins increased,while the Cyclin D1,Bcl-2,MMP-3 proteins were down-regulated in Bel-7402 and Bel-7402-miR-320a cells induced by ribonucleic acid Ⅱ.Conclusions The expression of miR-320a is lower in HCC cells than that in normal cell line.While ribonucleic acid Ⅱ could promote the apoptosis of liver cancer cells by arresting the cell cycle protein expression of Cyclin D1,activating p53 signaling pathway,down-regulating Bcl-2,up-regulating Bax and destroying Bcl-2/Bax proportions,and inhibiting the migration and invasion of HCC cells by downregulating MMP-3.Overexpression of miR-320a could increase the sensitivity and boost the pharmacological effects of ribonucleic acid Ⅱ on HCC cells.
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Objective To investigate the effect of evodiamine on proliferation of HCT-116 in balb/c nude mice, and to explore possible mechanism. Methods HCT-116 cells were injected into the right armpit of 4 week old Balb/c nude mice, the feeding had been executed at the time of the diameter of the xenografted tumor reached 0.5 cm,at the dose of 3 mg/kg (Evo), body weight and tumor diameter had been tested every three days, and made the curve of body weight and tumor diameter of the mice. All the mice were sacrificed after 22 days of feed-ing,and harvested the xenografted tumors. The morphological difference of the two groups tumor were identified by HE staining,the expression of HDAC3, NF-κB and p53 protein were detected by IHC and Western blot. Results Compared with the control groups, the volume and weight of the tumors in Evo groups were significantly lighter, and the body weight of the nude mice were heavier,the tumor cells in Evo groups were shrink,deeply staining nu-celus and their abnormal mitoses were fewer,the expression of NF-κB and p53 were increased but HDAC3 was de-creased in xenografted tumors treated with Evo(P<0.05). Conclusions Evo can change the expression of NF-κB and p53 by down-regulating HDAC3,and inhibit the proliferation of HCT-116 cells line in vivo.
ABSTRACT
Objective To investigate the effect of evodiamine on proliferation of HCT-116 in balb/c nude mice, and to explore possible mechanism. Methods HCT-116 cells were injected into the right armpit of 4 week old Balb/c nude mice, the feeding had been executed at the time of the diameter of the xenografted tumor reached 0.5 cm,at the dose of 3 mg/kg (Evo), body weight and tumor diameter had been tested every three days, and made the curve of body weight and tumor diameter of the mice. All the mice were sacrificed after 22 days of feed-ing,and harvested the xenografted tumors. The morphological difference of the two groups tumor were identified by HE staining,the expression of HDAC3, NF-κB and p53 protein were detected by IHC and Western blot. Results Compared with the control groups, the volume and weight of the tumors in Evo groups were significantly lighter, and the body weight of the nude mice were heavier,the tumor cells in Evo groups were shrink,deeply staining nu-celus and their abnormal mitoses were fewer,the expression of NF-κB and p53 were increased but HDAC3 was de-creased in xenografted tumors treated with Evo(P<0.05). Conclusions Evo can change the expression of NF-κB and p53 by down-regulating HDAC3,and inhibit the proliferation of HCT-116 cells line in vivo.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the protective efficacy of propofol against paraquat induced lung injury.</p><p><b>METHODS</b>One hundred and twenty-eight male Wistar rats were randomizedly divided into three groups: the control group (n = 8), the intoxication group (n = 60) and the propofol group (n = 60). One hundred and twenty rats were once administered with 5 mg/kg paraquat (PQ) by the intragastrical injection to establish the model of PQ induced lung injury. The propofol of 10 mg/kg was administered intraperitoneally in the propofol group (60 rats) twice a day for four consecutive days one hour after the rats were intoxicated while the normal saline of the same amount as propofol in the propofol group was administered in the intoxication group (60 rats) one hour after the rats were intoxicated. The intragastrical injection of 1 mg/kg normal saline was administered once in the control group (8 rats). On the first, the third, the seventh, the 14th and the 28th day after treating, the level of malondialdehyde (MDA) in plasma, bronchoalveolar lavage fluid (BALF) and lung homogenate, and the content of hydroxyproline (HPY) in lung homogenate, the cell count of BALF were detected. Meanwhile, pathological changes of lung were examined under optical microscope.</p><p><b>RESULTS</b>The level of MDA in plasma on the first, the third and the seventh day and in BALF and lung homogenate on the first and the third day in the propofol group [in plasma: (4.31 +/- 0.94), (4.04 +/- 0.87) and (3.24 +/- 1.14) nmol/ml; in BALF: (3.47 +/- 1.09) and (2.79 +/- 1.11) nmol/ml; in lung homogenate: (7.54 +/- 0.63) and (8.41 +/- 1.23) nmol/ml] were significantly lower than those in the intoxication group [in plasma: (10.15 +/- 3.15), (6.97 +/- 1.6 5) and (5.44 +/- 0.66) nmol/ml; in BALF: (5.58 +/- 1.19) and (4.86 +/- 1.89) nmol/ml; in lung homogenate: (10.20 +/- 2.43) and (10.71 +/- 171) nmol/ml, P < 0.05 or P < 0.01]. The total cell count of BALF on the first, the third and the seventh day after intoxication in the propofol group was significantly less than that in the intoxication group respectively (P < 0.05). The histological changes such as alveolar edema, hemorrhage and inflammatory cell infiltration in the propofol group were less than those in the PQ group.</p><p><b>CONCLUSION</b>Propofol could reduce the level of MDA and relieve paraquat induced lung injury.</p>