Biomedical subjects

Ke Liu

Publications and source records attributed to Ke Liu.

At least 37 records · Page 2Linked to original sources

PubMed2006

[Treatment of intra-articular fracture with absorbable screws and rods].

OBJECTIVE: To assess the treatment effect of intra-articular fracture with absorbable screws and rods. METHODS: From June 1998 to August 2004, 35 patients with intra-articular fracture were treated by absorbable screws and rods made of self-reinforced polyglycolic acid (SR-PGA) and self-reinforced poly-L-Lactic acid (SR-PLLA). Of 35 patients, 30 were males and 5 were females (aged from 4 to 62 years). All cases had intra-articular or periarticular fracture. The interval between injury and operation was 3 hours to 29 days. Fracture were fixed with full thread screws of SR-PGA in 9 cases, with tensile screws of SR-PLLA in 26 cases, with rods of SR-PLLA in 15 cases. Bone traction or plaster external fixation were carried out postoperatively. RESULTS: The patients were followed from 3 months to 60 months with an average of 28 months. The wounds healed by first intention, and the healing time of bone was 1-3 months. No dislocation, infection and local effusion occurred. Functional recovery was satisfactory. According to AASO articular function standard, the results were excellent in 26 cases, good in 7 cases, fair in 1 case, and poor in 1 case; the total excellent and good rate was 94.3%. CONCLUSION: Internal fixation of absorbable screws and rods are a perfect procedure in treating intra-articular and periarticular fracture, which can avoid the pain of taking out internal fixation materials because of second operation.

Absorbable Implants↗

PubMed2006

[Changes in inflammatory cascade response and its implication during cerebral ischemia/reperfusion in aged rats].

OBJECTIVE: To investigate the changes in expression of tumor necrosis factor-alpha(TNF-alpha), vascular cellular adhesive molecule-1 (VCAM-1), intercellular adhesion molecular-1 (ICAM-1) and its mRNA expression, and the pathogenetic mechanism of cerebral ischemia/reperfusion(I/R) in elderly. METHODS: Thirty six male young SD rats (5-6 months old) and 36 male aged SD rats (20-21 months old) were randomly divided into young sham operated group, young model group, aged sham operated group and aged model group, respectively. The two model groups were randomly divided into ischemia 3 hours (I 3 h), I/R 1, 3, 6, 12 days groups. There were 6 rats in each group. Focal cerebral I/R model was replicated with middle cerebral artery occlusion (MCAO). The changes of the nervous dysfunction score, the water content of cerebral constitution and the expression of TNF-alpha, VCAM-1, ICAM-1 and ICAM-1 mRNA were observed at each time point. RESULTS: The expression of TNF-alpha in the aged sham operated group were higher than that of the young sham operated group. The nervous dysfunction score (I 3 h and I/R 1-12 d), the water content of cerebral constitution (I/R 1-6 d), the expression of TNF-alpha (I 3 h and I/R 1-6 d), VCAM-1 (I 3 h and I/R 1 d), ICAM-1 (I 3 h and I/R 1-6 d) and ICAM-1 mRNA (I 3 h and I/R 1-12 d) in young model group and aged model group were higher than those of the young sham operated group and the aged sham operated group respectively. The nervous dysfunction score (I 3 h, I/R 6 d), the expression of TNF-alpha (I/R 1, 3 d), VCAM-1 (I/R 3, 6 d), ICAM-1 (I 3 h, I/R 1 d) and ICAM-1 mRNA (I/R 1-6 d) in aged model group were higher than that of young model group. CONCLUSION: The cerebral I/R injury is correlated with the up regulation of TNF-alpha, VCAM-1,ICAM-1 and its mRNA expression. The cerebral I/R injury of aged rats is more serious than that of young rats which might be associated with up regulation of TNF-alpha, adhesion molecules expression with aging.

Age Factors↗

PubMed2006

[HSF1 inhibits heat stress-induced apoptosis in Raw264.7 macrophages].

OBJECTIVE: To observe the effect of heat shock factor 1 (HSF1) on heat stress-induced apoptosis in Raw264.7 macrophages. METHODS: Raw264.7 cells transfected with pcDNA3.1 and pcDNA3.1-HSF1 were exposed to heat stress (42.5 degrees C +/- 0.5 degrees C) for 1 h and recovered at 37 degrees C for 6, 9, 12, and 24 h respectively. Flow cytometry (FCM), Hoechst 33258 staining and DNA ladder assays were performed to assess the apoptosis. RESULTS: After heat stress, FCM showed that apoptotic cells were increased significantly and reached the peak at 9 h in Raw 264.7 cells transfected with pcDNA3.1, and were characterized with classical morphologic changes including apoptotic body and nuclear condensation. Agarose gel electrophoresis showed that "DNA ladder" could be observed clearly at 6, 9, and 12 h after the heat stress. But the overexpression of HSF1 could reduce the number of apoptotic cells and inhibit DNA fragmentation. CONCLUSION: HSF1 can inhibit heat stress-induced apoptosis in Raw264.7 macrophages.

Animals↗

PubMed2006

[Effect of HSP72 on acute injury of neonatal cardiomyocytes induced by oxidative stress].

OBJECTIVE: To explore the protective effect of HSP72 on the acute injury of cardiomyocyte induced by oxidative stress. METHODS: Cardiomyocytes of neonatal rats treated with heat shock (42 degrees C, 30 min, recovery for 6 h) to induce the expression of HSP72 and HSP72 antisense oligonucleotide was transformed to block the expression of HSP72. 0.5 mmol/L (final concentration) H2O2 was added into the culture medium to mimic oxidative stress, and to induce the acute injury of neonatal cardiomyocytes. The release of LDH and the total protein synthesis were applied to evaluate the injury of cardiomyocyte of neonatal rats. RESULTS: Oxidative stress could significantly increase the release of LDH, and inhibit the total protein synthesis. By inducing the expression of HSPs, heat shock pretreatment significantly reduced the release of LDH and relieved the oxidative stress-mediated inhibition of total protein synthesis. Moreover, HSP7-2 anti-sense oligonucleotide could remarkably block the protective effect of heat shock pretreatment on the cellular injuries induced by H2O2. CONCLUSION: HSP72 plays a most important role in the acute injury of cardiomyocyte mediated by oxidative stress.

Animals↗

PubMed2005

Characterization of the role of gamma2 R531G mutation in AMP-activated protein kinase in cardiac hypertrophy and Wolff-Parkinson-White syndrome.

AMP-activated protein kinase (AMPK) is the downstream component of a protein kinase cascade that plays a key role in the regulation of energy metabolism. In humans, mutations in the gamma2-subunit of AMPK cause cardiac hypertrophy associated with Wolff-Parkinson-White syndrome, characterized by ventricular preexcitation. The effect of these mutations on AMPK activity and in development of the disease is enigmatic. Here we report that transgenic mice with cardiac-specific expression of gamma2 harboring a mutation of arginine residue 531 to glycine (RG-TG) develop a striking cardiac phenotype by 4 wk of age, including hypertrophy, impaired contractile function, electrical conduction abnormalities, and marked glycogen accumulation. At this stage, AMPK activity isolated from hearts of RG-TG mice was almost completely abolished but could be restored after phosphorylation by an upstream AMPK kinase. At 1 wk of age, there was no detectable evidence of a cardiac phenotype, and AMPK activity in RG-TG hearts was similar to that in nontransgenic, control mice. We propose that mutations in gamma2 lead to suppression of total cardiac AMPK activity secondary to increased glycogen accumulation. The subsequent decrease in AMPK activity provides a mechanism that may explain the development of cardiac hypertrophy in this model.

AMP-Activated Protein Kinases↗

PubMed2005

Identification of a repressor in the first intron of the human alpha2(I) collagen gene (COL1A2).

The human and mouse genes that code for the alpha2 chain of collagen I (COL1A2 and Col1a2, respectively) share a common chromatin structure and nearly identical proximal promoter and far upstream enhancer sequences. Despite these homologies, species-specific differences have been reported regarding the function of individual cis-acting elements, such as the first intron sequence. In the present study, we have investigated the transcriptional contribution of the unique open chromatin site in the first intron of COL1A2 using a transgenic mouse model. DNase I footprinting identified a cluster of three distinct areas of nuclease protection (FI1-3) that span from nucleotides +647 to +760, relative to the transcription start site, and which contain consensus sequences for GATA and interferon regulatory factor (IRF) transcription factors. Gel mobility shift and chromatin immunoprecipitation assays corroborated this last finding by documenting binding of GATA-4 and IRF-1 and IRF-2 to the first intron sequence. Moreover, a short sequence encompassing the three footprints was found to inhibit expression of transgenic constructs containing the COL1A2 proximal promoter and far upstream enhancer in a position-independent manner. Mutations inserted into each of the footprints restored transgenic expression to different extents. These results therefore indicated that the unique open chromatin site of COL1A2 corresponds to a repressor, the activity of which seems to be mediated by the concerted action of GATA and IRF proteins. More generally, the study reiterated the existence of species-specific difference in the regulatory networks of the mammalian alpha2(I) collagen coding genes.

Animals↗

PubMed2005

One step isolation and purification of liquiritigenin and isoliquiritigenin from Glycyrrhiza uralensis Risch. using high-speed counter-current chromatography.

High-speed counter-current chromatography (HSCCC) technique in semi-preparative scale has been successfully applied to the separation of bioactive flavonoid compounds, liquiritigenin and isoliquiritigenin in one step from the crude extract of Glycyrrhiza uralensis Risch. The HSCCC was performed using a two-phase solvent system composed of n-hexane-ethyl acetate-methanol-acetonitrile-water (2:2:1:0.6:2, v/v). Yields of liquiritigenin (98.9% purity) and isoliquiritigenin (98.3% purity) obtained were 0.52% and 0.32%. Chemical structures of the purified liquiritigenin and isoliquiritigenin were identified by electrospray ionization-MS (ESI-MS) and NMR analysis.

Chalcone↗

PubMed2005

The sphingoid long chain base phytosphingosine activates AGC-type protein kinases in Saccharomyces cerevisiae including Ypk1, Ypk2, and Sch9.

The Pkh1 protein kinase of Saccharomyces cerevisiae, a homolog of the mammalian 3-phosphoinositide-dependent kinase (PDK1), regulates downstream AGC-type protein kinases including Ypk1/2 and Pkc1, which control cell wall integrity, growth, and other processes. Phytosphingosine (PHS), a sphingoid long chain base, is hypothesized to be a lipid activator of Pkh1 and thereby controls the activity of Ypk1/2. Here we present biochemical evidence supporting this hypothesis, and in addition we demonstrate that PHS also stimulates autophosphorylation and activation of Ypk1/2. Greatest stimulation of Ypk1/2 phosphorylation and activity are achieved by inclusion of both PHS and Pkh1 in an in vitro kinase reaction. We also demonstrate for the first time that Pkh1 phosphorylates the Sch9 protein kinase in vitro and that such phosphorylation is stimulated by PHS. This is the first biochemical demonstration of Sch9 activators, and the results further support roles for long chain bases in heat stress resistance in addition to implying roles in chronological aging and cell size determination, since Sch9 functions in these processes. Thus, our data support a model in which PHS, rather than simply being an upstream activator of Pkh1, also activates kinases that are downstream targets of Pkh1 including Ypk1/2 and Sch9.

3-Phosphoinositide-Dependent Protein Kinases↗

PubMed2005

Neuroprotective effect of 20(S)-ginsenoside Rg3 on cerebral ischemia in rats.

This study was conducted to investigate the neuroprotective effects of 20(S)-ginsenoside Rg3 on focal cerebral ischemia in rats. Middle cerebral artery occlusion (MCAO) model in male Wistar-Kyoto (WKY) rats was employed. The behavioral tests were used to evaluate the damage to central nervous system. The infarct area of brain was assessed in the brain slices stained with 2,3,5-triphenyltetrazolium chloride (TTC). Hydrogen clearance techniques were used to monitor regional cerebral blood flow (rCBF), spectrophotometric assay methods were used to determine the activities of superoxide dismutase (SOD) and glutathione-peroxidase (GSH-Px), contents of malondialdehyde (MDA) and adenosine triphosphate (ATP) of the brain. Furthermore, the respiratory control ratio (RCR=State 3/State 4) was assessed in the brain mitochondria. The results showed that sublingual vein injection of 20(S)-ginsenoside Rg3 at doses of 10 and 5 mg kg(-1), but not 2.5 mg kg(-1) exhibited significant neuroprotective effects on rats against focal cerebral ischemic injury by markedly decreasing neurological deficit scores, reducing the infarct area and enhancing the rCBF compared with the control group. At the same time, 20(S)-ginsenoside Rg3 significantly improved mitochondrial energy metabolism, antagonized decreases in SOD and GSH-Px activities and increase in MDA level induced by cerebral ischemia. All these findings suggest that 20(S)-ginsenoside Rg3 might provide neuroprotection against the cerebral ischemia-induced injury in rat brain through reducing lipid peroxides, scavenging free radicals and improving the energy metabolism.

Adenosine Triphosphate↗

PubMed2005

Escin: inhibiting inflammation and promoting gastrointestinal transit to attenuate formation of postoperative adhesions.

Postoperative peritoneal adhesions are common, serious complications of general abdominal and gynecologic surgery that can lead to chronic abdominal pain, intestinal obstruction, and infertility. As yet, there are no ideal drugs that may be prescribed for patients to prevent adhesion formation effectively. In this study the effects of escin, a natural drug, on the various steps of adhesion formation were investigated. The effects of escin on increased vascular permeability induced by acetic acid in a mouse model of acute inflammation, granuloma formation in a subchronic inflammatory rat model, gastrointestinal transit in rats with intestinal paralysis, intestinal motility in postoperative patients, and postoperative adhesion formation in a rat model were observed. It was shown that escin could inhibit acute inflammation and granuloma formation, cause acceleration of gastrointestinal transit, help recover intestinal motility, and attenuate the formation of postoperative adhesions. The findings suggest that escin attenuates the formation of postoperative adhesions by inhibiting inflammation and promoting gastrointestinal transit. Thus it may be concluded that both inhibition of inflammation and increased gastrointestinal motility during the early postoperative period have a positive effect on decreasing the formation of adhesions.

Adult↗

PubMed2005

Therapeutic effects of hydroxysafflor yellow A on focal cerebral ischemic injury in rats and its primary mechanisms.

The therapeutic effects of hydroxysafflor yellow A (HSYA), extracted from Carthamus tinctorius. L, on focal cerebral ischemic injury in rats and its related mechanisms have been investigated. Focal cerebral ischemia in rats were made by inserting a monofilament suture into internal carotid artery to block the origin of the middle cerebral artery and administrated by HSYA via sublingular vein injection in doses of 1.5, 3.0, 6.0 mg kg(-1) at 30 min after the onset of ischemia, in comparison with the potency of nimodipine at a dose of 0.2 mg kg(-1). Then, 24 h later, the evaluation for neurological deficit scores of the rats were recorded and postmortem infarct areas determined by quantitative image analysis. At the end of the experiment, blood samples were taken to determine plasma 6-Keto-PGF1alpha/TXB2 by radioimmunoassays and blood rheological parameters. The effects exerted by HSYA on thrombosis formation by artery vein by-pass method and ADP-induced platelet aggregation in vivo and in vitro were investigated, respectively. The results indicated that more than 30% of the area of ischemic cerebrum was observed in the ischemic model group. HSYA dose-dependently improved the neurological deficit scores and reduced the cerebral infarct area, and HSYA bore a similarity in potency of the therapeutic effects on focal cerebral ischemia to nimodipine. The inhibition rates of thrombosis formation by HSYA at the designated doses were 20.3%, 43.6% and 54.2%, respectively, compared with saline-treated group. Inhibitory activities of HSYA were observed on ADP-induced platelets aggregation in a dose-dependent manner, and the maximum inhibitory aggregation rate of HSYA was 41.8%. HSYA provided a suppressive effect on production of TXA2 without significant effect on plasma PGI2 concentrations. Blood rheological parameters were markedly improved by HSYA, such as whole blood viscosity (from 21.71 +/- 4.77 to 11.61 +/- 0.90 mPa.s), plasma viscosity (from 2.73 +/- 0.53 to 1.42 +/- 0.07 mPa.s), deformability (from 0.66 +/- 0.26 to 0.77 +/- 0.33) and aggregation of erythrocyte (from 3.24 +/- 0.41 to 2.57 +/- 0.30), but no significant effect of HSYA on homatocrit was found (from 51.38 +/- 4.68% to 49.91 +/- 2.32%). HSYA appears to be a good potential agent to treat focal cerebral ischemia, and the underlying mechanisms exerted by HSYA might be involved in its inhibitory effects on thrombosis formation and platelet aggregation as well as its beneficial action on regulation of PGI2/TXA2 and blood rheological changes in rats.

Animals↗

PubMed2005

Desmosomal cadherin misexpression alters beta-catenin stability and epidermal differentiation.

Desmosomal adhesion is important for the integrity and protective barrier function of the epidermis and is disregulated during carcinogenesis. Strong adhesion between keratinocytes is conferred by the desmosomal cadherins, desmocollin (Dsc) and desmoglein. These constitute two gene families, members of which are differentially expressed in epidermal strata. It has been suggested that this stratum-specific expression regulates keratinocyte differentiation. We tested this hypothesis by misdirecting the expression of the basally abundant desmosomal cadherins Dsc3a and Dsc3b to suprabasal differentiating keratinocytes in transgenic mice. No phenotype was apparent until adulthood, when mice developed variable ventral alopecia and had altered keratinocyte differentiation within affected areas. The follicular changes were reminiscent of changes in transgenic mice with an altered beta-catenin stability. Stabilized beta-catenin and increased beta-catenin transcriptional activity were demonstrated in transgenic mice prior to the phenotypic change and in transgenic keratinocytes as a consequence of transgene expression. Hence, a link between desmosomal cadherins and beta-catenin stability and signaling was demonstrated, and it was shown that desmocollin cadherin expression can affect keratinocyte differentiation. Furthermore, the first function for a "b-type" desmocollin cadherin was demonstrated.

Alopecia↗

PubMed2005

[Effect of nucleolin down-regulation on the proliferation and apoptosis in C2C12 cells].

OBJECTIVE: To clarify the effect of nucleolin on the proliferation and apoptosis in C2C12 cells. METHODS: After inhibiting the expression of nucleolin using antisense oligonucleotides, the cellular proliferation was determined by MTT, and the apoptosis was detected by flow cytometry (FCM) assays and DNA ladder assays. RESULTS: After being transfected with antisense oligonucleotides for 24 hours, Western blotting showed that the expression of nucleolin was repressed significantly. In cells treated with antisense oligonucleotides, the cellular proliferation was obviously inhibited; the apoptotic cell increased significantly; and the "DNA ladder" was clearly observed. But the sense and random oligonucleotides had no effect on the cellular proliferation and apoptosis. CONCLUSION: The down-regulation of nucleolin can inhibit the cellular proliferation and initiate the apoptosis in C2C12cells.

Animals↗

PubMed2005

[Oxidative stress-induced accumulation of heat shock protein 70 within nucleolus].

OBJECTIVE: To investigate the effect of oxidative stress on the accumulation of heat shock protein 70 (HSP70) within C2C12 myogenic cells. METHODS: Heat shock response (42 degrees C for 1 h and recovery for 12 h at 37 degrees C) was used to induce the expression of heat shock protein 70. We constructed a recombinant plasmid of HSP70 with enhanced green fluorescent protein (EGFP). After being transfected transiently into C2C12 cells, immunoblotting was used to detect the expression of HSP70 induced by heat shock response and transfection. Immunocytochemistry, fluorescent microscopy and immunoblotting were used to detect the translocation of HSP70. RESULTS: Immunoblotting showed that the overexpression of HSP70 was induced by heat shock response and transient transfenction. HSP70 localized within the cytoplasm of the normal cells, but HSP70 translocated from the cytoplasm to the nucleus and the nucleolus at 1 h after the treatment of oxidative stress (0.5 mmol/L H2O2) by using immunocytochemistry, fluorescent microscopy and immunoblotting for cellular partial proteins. CONCLUSION: Oxidative stress may induce the accumulation of heat shock protein 70 within the nucleolus.

Cell Nucleolus↗

PubMed2005

[Relationship of changes in basement membrane of microvessels after cerebral ischemia/reperfusion and plasminogen activator system in aged rats].

OBJECTIVE: To study the relationship of changes in basement membrane of cerebral micro-vessels and plasminogen activator system after cerebral ischemia/reperfusion (I/R) injury in aged rats. METHODS: Middle cerebral artery occlusion (MCAO) was produced by the introduction of a thread. Rats were divided randomly into sham-operation group with young rats (cerebral ischemia 3 hours and I/R 6, 12, 24, 72, 144 hours groups), sham-operation group and I/R groups in aged rats (cerebral ischemia 3 hours and I/R 6, 12, 24, 72, 144 hours groups). Immunohistochemical technique, zymogram analysis, and reverse zymogram analysis were used to study changes in basement membrane structure of cerebral-cortex microvessel, type IV collagen (Col IV) and laminin (LN) contents, and plasminogen activator system in every group. RESULTS: With the increase of age, Col IV and LN contents of the microvessel basement membrane increased. With prolongation of I/R, the contents of Col IV and LN decreased in both young and aged rats, while the contents of tissue plasminogen activator (t-PA), urokinase plasminogen (u-PA) and plasminogen activator inhibitor (PAI-1) expression increased at the beginning and decreased subsequently. Compared with young groups, Col IV (ischemia 3 hours-I/R 12 hours), LN (ischemia 3 hours-I/R 24 hours), t-PA (I/R 6-24 hours) and u-PA (I/R 12-144 hours) expression levels were higher in aged rats, but PAI-1 (I/R 12 and 24 hours) expression was lower. In addition, changes in PAI-1 contents as determined with reverse zymogram analysis method coincided with its immunoexpression. CONCLUSION: With the increase of age, alterations in constituents of cerebro-microvessel basement membrane (Col IV and LN) increased. Injury to cerebro-microvessel basement membrane resulted in more serious changes in aged rats compared with the young rats. Changes in cerebro-microvessel basement membrane after I/R injury in the aged SD rats is related to change in plasminogen activator system.

Age Factors↗

PubMed2005

[Characteristics and expression of Mip5, a novel gene associated with myocardial ischemia/reperfusion in rats].

OBJECTIVE: To determine the characteristics of a novel gene Mip5 (GenBank accession number AY553870) and its expression under physiological and pathological conditions. METHODS: The characteristics of Mip5 were analyzed by bioinformatic programs including BLAST, spidey, psort, ClustalW and so on. RT-PCR was performed to detect Mip5 expression. RESULTS: Bioinformatic analysis showed that Mip5 gene lied in the 13th chromosome and contained 8 exons and 7 introns, its open reading frame contained 909 bp and its protein production was 302 amino acid residues including 6 kelth domains. Under normal conditions, MIP5 expressed abundantly in the heart, brain and kidney, but its expression could not be detected in the liver and muscle. Expression of Mip5 gene was increased significantly after ischemia-reperfusion compared with the sham groups, and reached its peak at 3 h and recovered at 12 h after the reperfusion. Conclusion Mip5 gene is a novel gene containing a putative open reading frame of 302 amino acids residues and may play an important role in rat cardiomyocytes suffering ischemia processing.

Amino Acid Sequence↗

PubMed2005

[Alkaline-degradation products of ginsenosides from leaves and stems of Panax quinquefolium].

AIM: To study the alkaline-degradation products of ginsenosides from leaves and stems of Panax quinquefolium L. METHODS: Isolation and purification were carried out on silica gel and HPLC; the structures of chemical constituents were elucidated by spectral analysis. RESULTS: From the alkaline-degradation products, nine compounds were identified as: 20 (S) -protopanaxadiol (I), 20 (S) -dammar-25 (26)-ene-3beta, 12beta, 20-triol (II), 24 (R) -ocotillol (III), 20 (S) -protopanaxatriol (IV), 20 (S) -dammar-25 (26)-ene-3beta, 6alpha, 12beta, 20-tetrol (V), dammar-20 (21), 24-diene-3beta, 12beta-diol (VI), dammar-20(21), 24-diene-3beta, 6alpha, 12beta-triol (VII), 20 (S), 24 (S) -dammar-25 (26) -ene-3beta, 6alpha, 12beta, 20, 24-pentanol (VIII), 20 (S) -dammar-23-ene-25-hydroperoxyl-3beta, 6alpha, 12beta, 20-tetrol (IX). CONCLUSION: The configuration of C20 position of ginsenosides was not changed by alkaline-degradation. The complete assignments of 1H and 13C NMR chemical shifts of four new compounds V, VII, VIII, IX, were acquired by means of 2D NMR spectra. Compound I showed antitumor effect on human colon carcinoma cells in vitro.

Antineoplastic Agents, Phytogenic↗

PubMed2005

[Protective effect of hydroxysafflor yellow A on experimental cerebral ischemia in rats].

AIM: To investigate the protective effect of hydroxysafflor yellow A (HSYA), a soluble element extracted from Carthamus tinctorius L., on focal cerebral ischemia in rats. METHODS: Focal cerebral ischemia in male Wistar-Kyoto (WKY) rats were induced by permanent middle cerebral artery occlusion (MCAO). Three doses of 1.5, 3.0 and 6.0 mg x kg(-1) of HSYA were administrated to three groups of rats, separately, via sublingular vein injection 30 min after the onset of ischemia. 24 h after ischemia in rats, neurological deficit scores were evaluated and the infarction area of brain was assessed by quantitative image analysis. The in vitro neuroprotective effect of HSYA was tested in cultured fetal cortical neurons exposed to glutamate and sodium cyanide (NaCN). RESULTS: HSYA at doses of 3.0 and 6.0 mg x kg(-1) exerted significant neuroprotective effects on rats with focal cerebral ischemic injury as expressed by neurological deficit scores and reduced the infarct area as compared with saline group, and the potency of HSYA at dose of 6.0 mg x kg(-1) was similar to that of 0.2 mg x kg(-1) of nimodipine. In vitro studies, HSYA significantly inhibited neurons damage induced by exposure to glutamate and NaCN in cultured fetal cortical cells. CONCLUSION: HSYA has potential neuroprotective action against focal cerebral ischemia in rats and cultured rat fetal cortical neurons as well.

Animals↗