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1.
Biomolecules & Therapeutics ; : 246-256, 2022.
Article in English | WPRIM | ID: wpr-925614

ABSTRACT

The present study focused on the potential mechanism of betulin (BT), a pentacyclic triterpenoid isolated from the bark of white birch (Betula pubescens), against chronic alcohol-induced lipid accumulation and metaflammation. AML-12 and RAW 264.7 cells were administered ethanol (EtOH), lipopolysaccharide (LPS) or BT. Male C57BL/6 mice were fed Lieber-DeCarli liquid diets containing 5% EtOH for 4 weeks, followed by single EtOH gavage on the last day and simultaneous treatment with BT (20 or 50 mg/ kg) by oral gavage once per day. In vitro, MTT showed that 0-25 mM EtOH and 0-25 μM BT had no toxic effect on AML-12 cells. BT could regulate sterolregulatory-element-binding protein 1 (SREBP1), lipin1/2, P2X7 receptor (P2X7r) and NOD-like receptor family, pyrin domains-containing protein 3 (NLRP3) expressions again EtOH-stimulation. Oil Red O staining also indicated that BT significantly reduced lipid accumulation in EtOH-stimulated AML-12 cells. Lipin1/2 deficiency indicated that BT might mediate lipin1/2 to regulate SREBP1 and P2X7r expression and further alleviate lipid accumulation and inflammation. In vivo, BT significantly alleviated histopathological changes, reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and triglyceride (TG) levels, and regulated lipin1/2, SREBP1, peroxisome proliferator activated receptor α/γ (PPARα/γ) and PGC-1α expression compared with the EtOH group. BT reduced the secretion of inflammatory factors and blocked the P2X7rNLRP3 signaling pathway. Collectively, BT attenuated lipid accumulation and metaflammation by regulating the lipin1/2-mediated P2X7r signaling pathway.

2.
Biomolecules & Therapeutics ; : 320-327, 2020.
Article | WPRIM | ID: wpr-830930

ABSTRACT

In current study, we aimed to investigate whether the gentiopicroside (GPS) derived from Gentiana manshurica Kitagawa could block the progression of alcoholic hepatic steatosis to fibrosis induced by chronic ethanol intake. C57BL/6 mice were fed an ethanol- containing Lieber-DeCarli diet for 4 weeks. LX-2 human hepatic stellate cells were treated with GPS 1 h prior to transforming growth factor-β (TGF-β) stimulation, and murine hepatocyte AML12 cells were pretreated by GPS 1 h prior to ethanol treatment. GPS inhibited the expression of type I collagen (collagen I), α-smooth muscle actin (α-SMA) and tissue inhibitor of metal protease 1 in ethanol-fed mouse livers with mild fibrosis. In addition, the imbalanced lipid metabolism induced by chronic ethanol-feeding was ameliorated by GPS pretreatment, characterized by the modulation of lipid accumulation. Consistently, GPS inhibited the expression of collagen I and α-SMA in LX-2 cells stimulated by TGF-β. Inhibition of lipid synthesis and promotion of oxidation by GPS were also confirmed in ethanol-treated AML12 cells. GPS could prevent hepatic steatosis advancing to the inception of a mild fibrosis caused by chronic alcohol exposure, suggesting GPS might be a promising therapy for targeting the early stage of alcoholic liver disease.

3.
Journal of Forensic Medicine ; (6): 319-323, 2019.
Article in English | WPRIM | ID: wpr-985015

ABSTRACT

Objective To investigate the application of the comprehensive use of multiple genetic markers in full and half sibling relationship testing through the identification of a case of suspected sibling relationship. Methods Genomic DNA were extracted from bloodstain samples from 4 subjects (ZHANG-1, ZHANG-2, male; ZHANG-3, ZHANG-4, female). Autosomal STR loci, X-STR, Y-STR loci and polymorphisms of mtDNA HV-Ⅰ and Ⅱwere genotyped by EX20 STR kit, X19 kit, Data Y24 STR kit, and Sanger sequencing, respectively. Results According to autosomal STR based IBS scoring results, full sibling relationships were indicated among ZHANG-2, ZHANG-3 and ZHANG-4, but those were not indicated between ZHANG-1 and ZHANG-2 or ZHANG-3 or ZHANG-4. According to autosomal STR based FSI and HSI, with ITO method and discriminant function method, full sibling relationships among ZHANG-2, ZHANG-3 and ZHANG-4 were indicated, and half sibling relationships between ZHANG-1 and ZHANG-2 or ZHANG-3 or ZHANG-4 were also indicated. X-STR and mtDNA sequencing results showed that all the 4 samples came from a same maternal line, and Y-STR results showed that ZHANG-1 and ZHANG-2 did not come from a same paternal line, which supported the half sibling relationship between ZHANG-1 and ZHANG-2 or ZHANG-3 or ZHANG-4, verified by parental genotype reconstruction based on autosomal STR genotyping. Conclusion For the identification of sibling relationships, it is effective to have reliable results with the mutual verification and support of multiple genetic markers (autosomal STR, sex chromosomal STR and mtDNA sequence) and calculations (IBS, ITO, discriminant function method and family reconstruction).


Subject(s)
Female , Humans , Male , Alleles , Chromosomes, Human, Y , DNA Fingerprinting , Forensic Genetics , Genetic Markers , Genotype , Microsatellite Repeats , Siblings
4.
Chinese Journal of Pharmacology and Toxicology ; (6): 338-339, 2018.
Article in Chinese | WPRIM | ID: wpr-705374

ABSTRACT

OBJECTIVE Dihydroquercetin(TAX)is the most abundant dihydroflavone found in on-ions,milk thistle and Douglas fir bark.We investigated whether TAX could inhibit the lipid accumulation in alcoholic liver steatosis in vivo and in vitro.METHODS An in vivo model was established by intragas-trically treating mice with ethanol,and an in vitro model was created by treating HepG2 cells with etha-nol.RESULTS TAX regulated Sterol Regulatory Element-binding Protein-1(SREBP1)and Acetyl CoA Carboxylase (ACC) expression via elevating Liver Kinase B1 (LKB1)/ AMP-activated Kinase (AMPK) phosphorylation. Also, TAX upregulated SIRT1 expression, which suppressed by ethanal intake. Suppression of Purinergic 2X7 receptor (P2x7R), nucleotide-binding oligomerization domain-like re-ceptor protein 3(NLRP3)and Cysteine protease-1(caspase-1)cleavage by TAX resulted in the inhibi-tion of Interleukin-1β(IL-1β) production and release. Additionally, TAX reduced lipogenesis and pro-moted lipid oxidation via the regulation of AMPK and ACC in ethanol-treated steatotic HepG2 cell.TAX downregulated IL-1β cleavage response to Lipopolysaccharides (LPS) plus adenosine triphosphate(ATP) stimulation in HepG2 cells. P2x7R deficiency attenuated lipid accumulation with increasing AMPK activity and decreasing SREBP1 expression in ethanol-treated HepG2 cells.CONCLUSION Our data showed that TAX exhibited the inhibitory properties on lipogenesis and hepatoprotective ca-pacity,indicating that TAX has therapeutic potential for preventing alcoholic liver steatosis.

5.
Chinese Journal of Pharmacology and Toxicology ; (6): 284-285, 2018.
Article in Chinese | WPRIM | ID: wpr-705302

ABSTRACT

OBJECTIVE To investigate toll-like receptor 4(TLR4)-related the regulation of Ornithog-alum caudatum extract(OCE)on inflammatory responses in lipopolysaccharide(LPS)activated macro-phages.METHODS Primary peritoneal macrophage,Raw 264.7,and THP-1 were incubated in 96-well plate for 24 h and treated with OCE of the concentration of 0-400 μg/ml for 4h.The viability of cells was measured by MTT assay.Specific concentrations of OCE were added into the medium of primary peri-toneal macrophage, Raw 264.7, and THP-1, respectively, then following with lipopolysaccharides (LPS). Cells were harvested and the total cellular protein and nuclear protein were extracted, and the protein content was determined using BCA protein assay Kit.The expressions of TLR4,inducible nitric oxide synthase(iNOS),cyclooxygenase 2(COX-2),α-inhibitor of NF-κB(IκB-α)and nuclear factor-κB (NF-κB)were assayed by Western blot.The expressions of interleukin-1α(IL-1α),interleukin-1β(IL-1β), interleukin-18(IL-18),and tumor necrosis factor-α(TNF-α)were measured by RT-PCR.RESULTS The results of MTT showed that OCE has no cytotoxicity in Raw 264.7 cells between 1.56 μg/ml and 400 μg/ml. Compared with normal group,the expressions of TLR4,iNOS,COX-2,NF-κB and IL-1α,IL-1β,IL-18, TNF-α,the level of nitric oxide(NO)were significantly increased by LPS stimulation,while OCE pretreat-ment reduced these increase induced by LPS. However, OCE pretreatment reversed the reduction of IκB-α after LPS stimulation.CONCLUSION OCE might suppress TLR4 expression and block the inflamma-tion process of NF-κB and iNOS,further decrease the expression of COX-2 and inhibit the release of inflammatory factors.

6.
Chinese Journal of Pharmacology and Toxicology ; (6): 276-276, 2018.
Article in Chinese | WPRIM | ID: wpr-705290

ABSTRACT

OBJECTIVE The current study was designed to investigate the anti-steatosis effect of Pleurotus citrinopileatus extract (PC) and the underlying mechanism in vivo and in vitro. METHODS Acute and chronic alcoholic hepatosteatosis murine models and ethanol-treated HepG2 cells were applied. RESULTS In vitro,the anti-steatosis effect of PC was further confirmed via Nile red staining in HepG2 cells treated with ethanol.Both of acute and chronic alcohol-induced mice hepatosteatosis model,PC decreased serum aminotransferase and triglyceride accumulation. Upregulated sterol-regulatory element binding protein1(Srebp1),purinergic ligand-gated ion channel 7receptor(P2X7R)and downregulated sirtuin1 (SIRT1), adenosine 5′-monophosphate (AMP)-activated protein kinase α (AMPKα) caused by acute and chronic alcohol intake were modulated by PC.In ethanol-exposed HepG2 cells,PC reduced lipid accumulation in a concentration-dependent manner and exhibited superior ability in controlling lipid accumulation compared with metformin. CONCLUSION PC could abolish hepatic lipid accumulation through regulating SIRT1-AMPKα signaling in acute and chronic alcohol-induced hepatic steatosis.

7.
Chinese Journal of Pharmacology and Toxicology ; (6): 265-266, 2018.
Article in Chinese | WPRIM | ID: wpr-705275

ABSTRACT

OBJECTIVE Regulating P2x7R- NLRP3 inflammasome activation might be a potentialtherapeutic strategy to treat alcoholic hepatosteatosis. We investigated whether this process would be modulated by gentiopicroside (GPS), which is attributed to the bitterness of gentian root extract. METHODSAn in vivo model was established by intragastrically treating mice with ethanol, and an in vitro modelwas created by treating HepG2 cells with ethanol or treating RAW 264.7 macrophages and murinebone marrow- derived macrophages (BMDMs) with lipopolysaccharides (LPS) plus adenosine triphos-phate (ATP). RESULTS In alcoholic hepatosteatotic mice model, GPS decreased serum aminotrans-ferase and triglyceride accumulation. GPS regulated sterol regulatory element-binding protein-1 (Srebp1),peroxisome proliferators- actived receptors α (PPARα) and acetyl CoA carboxylase (ACC) expressionvia elevating liver kinase B1 (LKB1)/AMP-activated Kinase (AMPK). Suppression of nucleotide-bindingoligomerization domain-like receptor protein 3 (NLRP3), caspase-1 and expression by GPS resulted inthe inhibition of interleukin-1β (IL-1β) production. In ethanol-exposed HepG2 cells, GPS reduced lipo-genesis and promoted lipid oxidation via P2x7R- NLRP3 inflammasome activation. P2x7R silencingenhanced AMPK activity, and reduced Srebp1 expression in ethanol-treated hepatocytes. GPS down-regulated P2x7R-mediated inflammatory response to extracellular ATP in LPS-primed RAW 264.7 macro-phages and BMDMs. Additionally, P2x7R deficiency attenuated IL- 1β cleavage in RAW 264.7 macro-phages, and GPS further suppressed IL-1β cleavage. CONCLUSION Activation of LKB1/AMPK signalingby GPS might be mediated by P2x7R-NLRP3 inflammasome, suggesting a therapeutic utility of P2x7Rblockade in alcoholic hepatosteatosis treatment.

8.
Journal of Xinxiang Medical College ; (12): 57-60, 2018.
Article in Chinese | WPRIM | ID: wpr-699471

ABSTRACT

Objective To compare the effect of ketamine and sufentanyl on respiratory depression induced by propofol in pediatric patients.Methods Sixty children with taplipes equines in the Department of Pediatric Orthopedics,the Third Affiliated Hospital of Zhengzhou University from February 2014 to August 2015 were selected and divided into ketamine group,sufentanil group and control group,with 20 patients in each group.The patients in ketamine group were given ketamine 1.50 mg· kg-1 by intravenous injection and maintained with ketamine 0.75 mg · kg-1 · h-1 by pump infusion;the patients in sufentanil group were given sufentanil 0.2 μg · kg-1 by intravenous injection and maintained with sufentanil 0.1 μg · kg-1 · h-1 by pump infusion;the patients in control group were given the same volume of saline.The initial plasma concentration of propofol in ketamine group,sufentanil group and control group was 1.1 mg · L-1,and the ratio between the two successive concentration gradients was 1.1.It was defined as positive when patients developed respiration depression.The bispectral index (BIS) and the observer's assessment of alertness/sedation (OAA/S) score of patients in the three groups were recorded at the time point of intravenous infusion ketamine or sufentanil (T1),3 min after propofol target controlled infusion (TCI) (T2),5 min after propofol TCI (T3) and after the target effect-site and plasma concentrations were balanced(T4).The target effect-site concentration was recorded when the BIS dropped to 65 or OAA/S score was 3.The median effective concentration(EC50) and its 95% confidence interval (CI) of propofol inducing respiratory depression were calculated.Results There was no statistic difference in BIS and OAA/S scores of patients at the time point of T1 among the three group(P > 0.05);the BIS and OAA/S scores of patients in ketamine group and sufentanil group were significantly lower than those in the control group at the time point of T2,T3 and T4 (P < 0.05);the BIS and OAA/S scores of patients in ketamine group were significantly lower than those in the sufentanil group at the time point of T2,T3,T4 (P < 0.05).The EC50 and its 95 % CI of respiratory depression induced by propofol in ketamine group,sufentanil group and the control group were 1.75 (1.56-2.34),1.86 (1.47-2.23),2.82 (2.56-3.02) mg · L-1 respectively.The EC50 of patients in ketamine group and sufentanil group was significantly lower than that in control group (P < 0.05),but there was no statistic difference in EC50 of patients between the ketamine group and sufentanil group (P > 0.05).Conclusion Both ketamine and sufentanil can increase the EC50 of respiratory depression induced by propofol in pediatric patients,but the effects of both drugs are the same.Ketamine and sufentanil can reduce the BIS and OAA/S scores of patients,enhance the sedation efficacy of propofol,and the effect of ketamine is better than sufentanil.

9.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 576-580, 2013.
Article in Chinese | WPRIM | ID: wpr-275882

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the DNA damage of splenic lymphocytes in pregnant mice exposed to carbon disulfide (CS2) in the implantation phase and to explore the mechanism of abnormal implantation induced by CS2 from the perspective of immune injury.</p><p><b>METHODS</b>Mice were exposed to CS2 at different doses or at different time points in the implantation phase to establish model 1 and model 2. For model 1, mice were assigned to four groups to receive a single intraperitoneal injection of low-dose CS2 (0.1 LD50, 157.8 mg/kg), middle-dose CS2 (0.2 LD50, 315.7 mg/kg), and high-dose CS2 (0.4 LD50, 631.4 mg/kg) as well as an equal volume of olive oil (control) on gestational day (GD) 4. For model 2, mice were assigned to four groups to receive a single intraperitoneal injection of CS2 (0.4 LD50, 631.4 mg/kg) or an equal volume of olive oil (control) on GD3, GD4, GD5, and GD6. At the end, single cell suspension of splenic lymphocytes was prepared. Cell viability was measured by trypan blue staining, and the DNA damage of splenic lymphocytes was evaluated by alkaline single cell gel electrophoresis assay.</p><p><b>RESULTS</b>The middle-dose and high-dose exposure groups showed significantly more DNA damage of splenic lymphocytes than the control group (P < 0.01); there was significant regression relationship between indicators of DNA damage and exposure doses (P < 0.01). The GD3, GD4, GD5, and GD 6 exposure groups showed significantly more DNA damage of splenic lymphocytes than the control group (P < 0.01), and the GD 4 exposure group had the most DNA damage.</p><p><b>CONCLUSION</b>Exposure to CS2 in the implantation phase can induce DNA damage of splenic lymphocytes in pregnant mice, and the DNA damage was aggravated with the increase in CS2 concentration. GD4 may be the sensitive time point for DNA damage of splenic lymphocytes induced by CS2 in pregnant mice.</p>


Subject(s)
Animals , Female , Mice , Pregnancy , Carbon Disulfide , Toxicity , DNA Damage , Embryo Implantation , Lymphocytes , Spleen , Cell Biology
10.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 88-91, 2013.
Article in Chinese | WPRIM | ID: wpr-343700

ABSTRACT

<p><b>OBJECTIVE</b>To evaluate the effects of carbon disulfide (CS(2)) exposure during peri-implantation on the estrogen receptor-α (ER-α) expression in the uterus and serum level of estradiol (E(2)) in pregnant mice, and to explore the mechanism of embryotoxicity of CS(2).</p><p><b>METHODS</b>Healthy female mice were exposed to a single dose of CS(2) (631.4 mg/kg) or olive oil (solvent control) on gestational day (GD)3, GD4, GD5, or GD6. At different time points after exposure, the serum E(2) levels of the pregnant mice were measured by enzyme-linked immunosorbent assay, and the expression levels of ER-α in the uterus were measured by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot.</p><p><b>RESULTS</b>Compared with the control group, the GD3, GD4, GD5, and GD6 exposure groups showed significantly decreased serum E(2) levels on day 7 of gestation (P < 0.05); the GD3 and GD5 exposure groups showed significantly decreased serum E(2) levels on day 6 of gestation (P < 0.05). The expression level of ER-α in the GD 4 exposure group was 23.6% lower than that in the control group on day 5 of gestation, and the expression level of ER-α in the GD 5 exposure group was 72.9% lower than that in the control group on day 6 of gestation (P < 0.05); the GD 3 and GD 6 exposure groups showed lower expression levels of ER-α than the control group at any time point, but no significant difference was found (P > 0.05).</p><p><b>CONCLUSION</b>CS(2) exposure during peri-implantation can reduce the ER-α expression in the uterus and the serum level of E(2) in pregnant mice, which may be one of the mechanisms of embryotoxicity of CS(2).</p>


Subject(s)
Animals , Female , Mice , Pregnancy , Carbon Disulfide , Toxicity , Embryo Implantation , Estradiol , Blood , Estrogen Receptor alpha , Metabolism , Mice, Inbred Strains , Uterus , Metabolism
11.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 881-884, 2010.
Article in Chinese | WPRIM | ID: wpr-293799

ABSTRACT

<p><b>OBJECTIVE</b>To observe the effect of carbon disulfide (CS(2)) on the expression of matrix metalloproteinase (MMP)-2, MMP-9 in mouse embryo and uterus tissues and to explore the mechanism of embryo toxicity induced by CS(2).</p><p><b>METHODS</b>At the phases of follicular development and embryonic implantation which was subdivided into early-implantation phase and late-implantation phase, mice were intraperitoneally exposed to CS(2) (the dosage was 631.4 mg/kg, and the volume was 0.1ml/10 g body weight) for 2 consecutive days. All indicators were got at the ninth day in gestation, and the expression of MMP-2 and MMP-9 in embryo and uterus tissues was analyzed by gelatin zymography.</p><p><b>RESULTS</b>The number of implanted embryos significantly decreased after exposure at late-implantation phase (16.000 ± 12.166) compared with those of the control (30.700 ± 5.599, P < 0.05). Expression of MMP-2 and MMP-9 in embryos declined obviously at the three reproductive phases (P < 0.01), and the levels of MMP-2 and MMP-9 expression in embryos at the phases of late-implantation phase (0.6837 ± 0.0929, 0.7309 ± 0.0822) and follicular development (0.6222 ± 0.0997, 0.7520 ± 0.1068) were much lower than those of the control (1.0000 ± 0.0710, 1.0000 ± 0.0413, P < 0.01). Expression of MMP-2 and MMP-9 in uterus significantly increased at the phase of late-implantation (1.3153 ± 0.3032, 5.0210 ± 4.0307) compared with those of the control (1.0000 ± 0.1771, 1.0000 ± 0.0996, P < 0.01).</p><p><b>CONCLUSION</b>Embryo toxicity of CS(2) is more obvious at the phase of late-implantation. Exposure to CS(2) disturbs expression of MMP-2 and MMP-9 in embryo and uterus tissues, which might be one of the important factors contributed to embryo toxicity induced by CS(2).</p>


Subject(s)
Animals , Female , Mice , Pregnancy , Carbon Disulfide , Toxicity , Embryo Implantation , Embryo, Mammalian , Metabolism , Matrix Metalloproteinase 2 , Metabolism , Matrix Metalloproteinase 9 , Metabolism , Mice, Inbred Strains , Uterus , Metabolism
12.
Chinese Journal of Stomatology ; (12): 155-158, 2009.
Article in Chinese | WPRIM | ID: wpr-346714

ABSTRACT

<p><b>OBJECTIVE</b>To analyze the stress distribution in all-ceramic crowns when it was subjected to load.</p><p><b>METHODS</b>A 3D numerical model of the all-ceramic crown of the right mandibular first molar was generated from scanned CT images. Finite element analysis (FEA) was used to evaluate the stress distribution in the all-ceramic crown when it was subjected to 5 load conditions.</p><p><b>RESULTS</b>Stress distributions under 5 loading conditions were obtained. Stress concentrations were generally found near the loading areas at the veneer and at the lower surface of the core beneath the loading areas. In the 5 loading conditions, it was found that when the crown was loaded with vertical concentrated load, the tensile stresses around the shoulder areas were uniform, while stress concentration with maximum of 32.25 MPa was found at the shoulder areas in lingual-buccal direction when loads were applied at an angle of 10 degrees with the tooth axis on the buccal side. The masticatory load which was applied at 20 degrees with the tooth axis on the buccal side would cause stress concentration at the shoulder in mesial-distal direction. The maximum value could reach 11.29 MPa.</p><p><b>CONCLUSIONS</b>The occlusal surface of the all-ceramic crown must be trimmed to increase multiple contact zones with the opposite surfaces in antagonist teeth to avoid excessive concentrated stress that may cause crown failure.</p>


Subject(s)
Crowns , Dental Porcelain , Dental Stress Analysis , Methods , Finite Element Analysis , Materials Testing
13.
Journal of Experimental Hematology ; (6): 1279-1282, 2008.
Article in Chinese | WPRIM | ID: wpr-234250

ABSTRACT

The purpose of this study was to explore the mechanism of CAG regimen eliminating T-cell acute lymphoblastic leukemia (T-ALL) A3 cell line and evaluate the role of G-CSF/G-CSFR system in this process. The expression levels of G-CSFR on the A3 cell membrane were detected by flow cytometry. Cell cycle changes of A3 cells treated with different concentrations of G-CSF for 48 hours were examined by propidium iodide staining method. The inhibition and apoptosis rates of A3 cells treated with various combinations of G-CSF, cytarabine (Ara-C), aclarubicin (ACR) were analyzed by Cell Counting Kit and AnnexinV Kit, respectively. The results indicated that the expression level of G-CSFR on A3 cells was 94.2%. The proportion of A3 cells in S-phase rose concomitantly with the increasing of G-CSF concentrations within 0-20 ng/ml. After incubation with Ara-C and G-CSF for 48 hours, A3 cells were inhibited more obviously compared with incubation with Ara-C alone (p<0.05, Ara-C 10(-5) mol/L and 10(-6) mol/L). After incubation with Ara-C, ACR and G-CSF for 48 hours, the apoptotic rate of A3 cells was much more than that after incubation with Ara-C and ACR. It is concluded that the expression level of G-CSFR on A3 cells is high, G-CSF/G-CSFR system has a synergetic effect on eliminating A3 cells when administrated simultaneously with chemical agents. This effect is caused through driving more cells from G0 phase into S phase, increasing sensitivity of A3 cells to chemical drugs and inducing cell apoptosis which may be one of the mechanisms of CAG regimen eliminating A3 cells.


Subject(s)
Humans , Aclarubicin , Therapeutic Uses , Antineoplastic Combined Chemotherapy Protocols , Therapeutic Uses , Apoptosis , Cell Line, Tumor , Cell Proliferation , Cytarabine , Therapeutic Uses , Granulocyte Colony-Stimulating Factor , Therapeutic Uses , Precursor T-Cell Lymphoblastic Leukemia-Lymphoma , Drug Therapy , Pathology
14.
Kampo Medicine ; : 817-822, 1999.
Article in Japanese | WPRIM | ID: wpr-368278

ABSTRACT

Yokuinin, coix seed extract, has been used to regulate gastric functions and to reduce pathological water retention. This paper reports the effect of Yokuinin on controlling hydrarthrosis for patients with arthralgia. Seventeen patients who have had maintenance hemodialisis for an average of 12.7 years and who have suffered hydrarthrosis with arthralgia have been tested. There are 7 male and 10 female patients, with an average of age of 63.4. The hydrarthrosis of the patients resulted from dialysis arthropathy and gonarthrosis. The patients were provided with 3 to 6 tablets of Yokuinin (Yokuinin extract tablet “Kotaro”) a day, and the effect on hydrarthrosis was measured after 3 weeks. The dosage of Yokuinin was 0.33g in 3 tablets. Yokuinin was effective on 14 patients (hydrarthrosis was reduced), relatively effective on 2 patients, and not effective on one patient. This shows an efficacy rate of 82.8%. Arthralgia was reduced for 12 patients, and analgesia was seen in 3 patients. Effective reduction of hydrarthrosis by this medicine was observed: 5 cases out of 6 for patients with dialysis arthropathy (83.3%); 6 cases out of 7 for gonarthrosis (85.7%); and 3 cases of 4 for other diseases (75.0%)—a total of 82.8%. The patient for whom the drug was not effective was suffering from acute hydrarthrosis. Side effects were not observed except for indigestion and cramps. These results suggest that Yokuinin is an effective medicine to control hydrarthrosis with arthralgia for patients under hemodialysis.

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