Biomedical subjects

N Jiang

Publications and source records attributed to N Jiang.

At least 55 records · Page 3Linked to original sources

PubMed1998

[Establishment of partial gene expression map of 7q32 in nasopharyngeal carcinoma and primary culture normal nasopharyngeal epithelial cells].

OBJECTIVE: To establish partial gene expression map of 7q32 in nasopharyngeal carcinoma (NPC) cell line, tissues and primary culture normal nasopharyngeal epithelial cells. METHODS: We detected the expression of 20 ESTs at 7q32 in NPC cell line HNE1,13 NPC biopsies and primary culture normal nasopharyngeal epithelial cells using differential RT PCR and Northern hybridization. RESULTS: 8 ESTs (AA188181, AA13079,N27556, AA031919, N22721, H20825, T91284, AA001936) expressed equally in both of HNE1 and primary culture normal nasopharyngeal epithelial cells; 7 ESTs (T64215, AA025822, R60014,R80002,H06688, R60192,R95096) expressed in neither of them; 3 ESTs (H19830,W72688,AA130630) overexpressed in HNE1 ; and 2 ESTs (AA070437, H90882) overexpressed in primary culture normal nasopharyngeal epithelial cells. W72688 and H19830 each overexpressed in 77%(10/13) of NPC biopsies; AA070437 down-expressed in 30.7% of NPC biopsies. CONCLUSION: Partial gene expression map of 7q32 in nasopharyngeal carcinoma cell line ,tissues and primary culture normal nasopharyngeal epithelial cells has been established. The up-regulation of W72688, H19830 and down-regulation of AA070437 may be related to the occurrence of NPC.

Blotting, Northern↗

PubMed1998

Erythropoietin receptor and STAT5-specific pathways promote SKT6 cell hemoglobinization.

Erythrocyte production in mammals is known to depend on the exposure of committed progenitor cells to the glycoprotein hormone erythropoietin (Epo). In chimeric mice, gene disruption experiments have demonstrated a critical role for Epo signaling in development beyond the erythroid colony-forming unit (CFU-e) stage. However, whether this might include the possible Epo-specific induction of red blood cell differentiation events is largely unresolved. To address this issue, mechanisms of induced globin expression in Epo-responsive SKT6 cells have been investigated. Chimeric receptors containing an epidermal growth factor (EGF) receptor extracellular domain and varied Epo receptor cytoplasmic domains first were expressed stably at physiological levels in SKT6 cells, and their activities in mediating induced hemoglobinization were assayed. While activity was exerted by a full-length chimera (EE483), truncation to remove 7 of 8 carboxyl-terminal tyrosine sites (EE372) markedly enhanced differentiation signaling. Moreover, mutation of a STAT5 binding site in this construct (EE372-Y343F) inhibited induced globin expression and SKT6 cell hemoglobinization, as did the ectopic expression of dominant-negative forms of STAT5 in parental SKT6 cells. As in normal CFU-e, SKT6 cells also were shown to express functional receptors for stem cell factor (SCF). To further define possible specific requirements for differentiation signaling, effects of SCF on SKT6 cell hemoglobinization were tested. Interestingly, SCF not only failed to promote globin expression but inhibited this Epo-induced event in a dose-dependent, STAT5-independent fashion. Thus, effects of Epo on globin expression may depend specifically on STAT5-dependent events, and SCF normally may function to attenuate terminal differentiation while promoting CFU-e expansion.

Animals↗

PubMed1998

[G6PD gene mutations in Guangxi, China].

OBJECTIVE: Fifty-six G6PD-deficient male individuals of the Guangxi origin were investigated at the molecular level to understand the basis of G6PD deficiency. METHODS: PCR amplified the exons 2,5,6,7,8, 10,11,12 and 13 of the G6PD gene respectively, combined with ASO dot blot hybridization and restriction enzymes digestion methods to screen 10 common Chinese G6PD mutations. RESULTS: Six mutations were detected, namely cDNA1376(G-->T)(25.0%), cDNA1388(G-->A)(16.1%), cDNA95(A-->G)(19.8%), cDNA592 (C-->T)(7.1%), cDNA1024(C-->T)(1.8%) and cDNA392(G-->T) (1.8%). The unknown mutations accounted for 28.6%. cDNA1311(C-->T),cDNA1360(C-->T),cDNA835(A-->T), cDNA493(A-->G) and cDNA487(G-->A) were not discovered among the cases. CONCLUSION: The findings may provide some useful informations for physician scientists to get insight into the pathogenesis of G6PD deficiency so as to improve clinical diagnosis, prevention and cure of G6PD deficiency. The results may be of significance in anthropology and geneties as well.

Glucosephosphate Dehydrogenase↗

PubMed1998

Evidence that HetR protein is an unusual serine-type protease.

The hetR gene plays a very important role in cell differentiation of heterocystous cyanobacteria. To understand the mechanism of the hetR gene product in regulation of heterocyst differentiation, the recombinant HetR protein (rHetR) was overproduced in Escherichia coli. Purified rHetR was unstable and degraded easily in solution. Phenylmethanesulfonyl fluoride, a serine-type protease inhibitor, prevented the degradation and was shown to modify covalently rHetR. Dansyl fluoride (DnsF), another serine-type protease inhibitor, also covalently modifies rHetR as shown by electrophoresis and electroblotting of the labeled rHetR and by MS. The labeling of rHetR with phenylmethanesulfonyl fluoride and DnsF was at the same site of rHetR and required Ca2+. S179N-rHetR, a mutant protein from strain 216 of Anabaena PCC 7120, which cannot differentiate heterocysts because of the mutation, was also overproduced and characterized. Although S170N-rHetR still can be labeled with DnsF, no proteolysis was observed, suggesting that Ser179 is involved in proteolytic activity. DnsF-labeled rHetR was digested with trypsin, and the labeled peptide was isolated and sequenced. The labeled peptide matches a sequence from HetR. These results show that HetR is a protease.

Amino Acid Sequence↗

PubMed1998

Intact, injured, necrotic and apoptotic cells after focal cerebral ischemia in the rat.

Middle cerebral artery occlusion (MCAo) leads to brain cell death. However, quantitation of injured brain cells and inflammatory cells after MCAo has not been determined in the rat. Transient (2 h) MCAo was therefore induced in male Wistar rats by means of an intraluminal monofilament. Immunohistochemical and histochemical procedures performed at 46 h after MCAo were used to identify specific cellular populations in ischemic and control rats (n = 11). In the ischemic core of the lesion, approximately 24.7% of cells disappeared. Forty-four point eight percent of parenchymal cells consisted of intact (13.0%) or reversibly injured swollen (7.6%) and scalloped/shrunken dark (24.2%) cells. The percentage of irreversibly damaged cells was 55.2%, and included 49.9% necrotic cells (10.5% red and 39.4% ghost) and 5.4% apoptotic cells. In the inner boundary zone of the lesion, 15.9% of cells disappeared. Viable cells constituted 62.0% of all remaining cells. Neutrophils and macrophages were localized to this area. In the outer boundary zone of the lesion, 9.0% of cells disappeared. Viable cells constituted 91.6% of all remaining cells. The ratio of apoptotic to necrotic cells was 1:9, 1:6, 1:13 in the ischemic core, inner and outer boundary zones, respectively. Our data suggest the presence of three zones within the ischemic lesion: the core, and inner and outer boundaries. At 46 h after 2 h of MCAo the ischemic lesion is highly heterogeneous containing relatively large percentages of morphologically intact cells, suggesting the possibility of an extended window of therapeutic opportunity.

Animals↗

PubMed1998

Neutrophil inhibitory factor treatment of focal cerebral ischemia in the rat.

The present study was designed to determine whether a hookworm-derived recombinant neutrophil inhibitory factor (rNIF) is neuroprotective when administered after initiation of focal cerebral ischemia in the rat. We measured the rNIF dose-response on cerebral infarct volume, the therapeutic time window, the therapeutic response to permanent ischemia, and whether rNIF treatment delays the maturation of the ischemic lesion (2 days), or reduces cerebral infarct volume at 7 days after middle cerebral artery occlusion (MCAO). MCAO was induced by an insertion of intraluminal 4-0 monofilament nylon suture into internal carotid artery (n=195). We demonstrate a significant neuroprotective effect of rNIF administration 48 h after MCAO in a dose-dependent fashion when treatment was initiated upon reperfusion after 2 h MCAO and maintained until 48 h after MCAO. The beneficial effect was lost under conditions of permanent MCAO. The therapeutic time window is 4 h after MCAO. Brief treatment (6 h) is not sufficient to provide protection for the final ischemic damage. Continuous treatment with a high dose of rNIF for a long duration (7 days) is necessary to achieve maximum neuroprotection.

Animals↗

PubMed1998

The expression of P- and E-selectins in three models of middle cerebral artery occlusion.

The expression and localization of P- and E-selectins in rat brain (n=126) were examined using immunohistochemical techniques at various time points after induction of middle cerebral artery (MCA) occlusion in the suture, thrombotic and embolic models of stroke. Expression of P- or E-selectin was not observed in brain tissue of sham operated control rats (n=9). P-selectin immunoreactivity was detected as early as 15 min and decreased to control level at 1 h after the onset of the MCA occlusion in all three models. P-selectin then slightly increased at 2 h and peaked at 6 h after MCA occlusion. E-selectin immunoreactivity was first observed at 2 h and peaked at 6 h and 12 h of after MCA occlusion in all three models. P- and E-selectin immunoreactivity was colocalized with von Willebrand factor immunoreactive microvessels. 90.4+/-2.0% of all vessels expressing P-selectin immunoreactivity were 7.5 to 30.0 micron in diameter; 3.6+/-1.4% were contained in vessels smaller than 7.5 micron, and 6.0+/-1.8% were localized in vessels greater than 30.0 micron in diameter. The percent distribution of E-selectin immunoreactive vessels were 75.9+/-2.1% in vessels 7.5 to 30.0 micron in diameter; 23.6+/-2.2% were in vessels smaller than 7.5 micron, and 0.6+/-0.4% were localized in vessels greater than 30.0 micron in diameter. These findings indicate that the temporal profiles of P- and E-selectin expression are independent of these models of MCA occlusion and are consistent with the time course of selectin mediated leukocyte infiltration after focal cerebral ischemia in the rat.

Analysis of Variance↗

PubMed1998

Neuronal damage and plasticity identified by microtubule-associated protein 2, growth-associated protein 43, and cyclin D1 immunoreactivity after focal cerebral ischemia in rats.

BACKGROUND AND PURPOSE: An objective of therapeutic intervention after cerebral ischemia is to promote improved functional outcome. Improved outcome may be associated with a reduction of the volume of cerebral infarction and the promotion of cerebral plasticity. In the developing brain, neuronal growth is concomitant with expression of particular proteins, including microtubule-associated protein 2 (MAP-2), growth-associated protein 43 (GAP-43), and cyclin D1. In the present study we measured the expression of select proteins associated with neurite damage and plasticity (MAP-2 and GAP-43) as well as cell cycle (cyclin D1) after induction of focal cerebral ischemia in the rat. METHODS: Brains from rats (n=28) subjected to 2 hours of middle cerebral artery occlusion and 6 hours, 12 hours, and 2, 7, 14, 21, and 28 days (n=4 per time point) of reperfusion and control sham-operated (n=3) and normal (n=2) rats were processed by immunohistochemistry with antibodies raised against MAP-2, GAP-43, and cyclin D1. Double staining of these proteins for cellular colocalization was also performed. RESULTS: Loss of immunoreactivity of both MAP-2 and GAP-43 was observed in most damaged neurons in the ischemic core. In contrast, MAP-2, GAP-43, and cyclin D1 were selectively increased in morphologically intact or altered neurons localized to the ischemic core at an early stage (eg, 6 hours) of reperfusion and in the boundary zone to the ischemic core (penumbra) during longer reperfusion times. CONCLUSIONS: The selective expressions of the neuronal structural proteins (MAP-2 in dendrites and GAP-43 in axons) and the cyclin D1 cell cycle protein in neurons observed in the boundary zone to the ischemic core are suggestive of compensatory and repair mechanisms in ischemia-damaged neurons after transient focal cerebral ischemia.

Animals↗

PubMed1998

[Immunoprotection in guinea pigs using DNA recombinant plasmid rpDJt and expressed protein P68 in L. interrogans serovar lai].

Immunoprotection against the infection by Leptospira interrogans serogroup Icterohemorrhagiae serovar lai strain 017 was demonstrated in guinea pigs vaccinated with DNA recombinant plasmid rpDJt and expressed protein P68 derived from genomic library of Leptospira strain 017. Thirty days after active immunization, each group received intraperitoneally (1/2 dose) and subcutaneously (1/2 dose) inoculum of L. interrogans serovar lai stain 017; cultures were adjusted to 5 x 10(8) cells/ml. All guinea pigs were observed for 10 days after challenge. Survival (%) of P68 group was 100(7/7); P23 group was 75(3/4); group rpDJt was 77(10/13); group lack recombinant (control) pT7-7 was 25 (3/12), and group with whole-cell inactivated vaccine was 93(13/14). Although the protective antigen in the leptospires has yet to be determined, it is evident that expressed protein P68 conferred a high degree of immunoprotection in guinea pigs.

Animals↗

PubMed1998

[Allelic loss on chromosome 3p21-26 in nasopharyngeal carcinoma].

OBJECTIVE: To determine the frequency and extent of loss of heterozygosity (LOH) on chromosome 3p in nasopharyngeal carcinoma (NPC). METHODS: Sixteen loci on chromosome bands 3p21-26 in 24 tumors was studied by using microsatellite analysis. RESULTS: LOH on 3p21-26 was found in 16 of 24 tumors (66.7%). The highest frequency of the allelic loss was found in two adjacent loci D3S1620(50%, 11/22) and D3S1560 (50%, 9/18). Eight cases showed LOH in one contiguous region and 5 cases in more than one region. Sample 1, 3, 4, 7, 8, 10, 16, 17, 18, 19, and 22 had a contiguous stretch of allelic loss between D3S1297 and D3S1597. CONCLUSION: The smallest common LOH/deletion region seems likely to lie between D3S1620(3p26.2-26.3) and D3S1560(3p25.3). The allelic loss map defined here will facilitate finer mapping of putative tumor suppressor gene loci and positional cloning of such genes, which may play a role in carcinogenesis of NPC.

Adult↗

PubMed1998

[The mechanisms of hyperhomocysteinemia in coronary heart disease].

OBJECTIVE: To identify hyperhomocysteinemia (HHe) as a new and independent risk factor for coronary heart disease (CHD). METHODS: The association of coronary heart disease (CHD) and lipid, homocysteine (HCY) and the factors related to its metabolisms were examined. The mutation of the 677C-->T transition of MTHFR was determined by PCR-based assay. Whole blood and plasma folate (FA) and plasma vitamin B12(B12), as cofactors of those enzymes, were determined by radioimmunologic assay. Plasma HCY was determined by HPLC. RESULTS: Patients with CHD confirmed by coronary angiography had increased plasma HCY concentrations (17.1 +/- 3.6 mumol/L, 7.6 +/- 1.2 mumol/L). In patients with MI, HPT and family history (FH) of CHD, plasma HCY increased significantly. Plasma HCY concentrations had significant non-linear inverse relation with plasma FA and B12 concentrations. Homozygous mutants showed higher plasma HCY concentrations. Patients with CHD had increased serum CHOL and VLDL levels, but plasma HCY concentrations were not correlated with serum lipid levels. CONCLUSION: Hyperhomocysteinemia is an independent risk factor for coronary heart disease.

Adult↗

PubMed1997

Apoptosis and protein expression after focal cerebral ischemia in rat.

We used double staining histochemistry to investigate the relationship between apoptotic cell death and selective protein expression associated with DNA damage (p53, Bax, MDM2, Gadd45), DNA repair (PCNA) and cell cycle proteins (cyclin A, cyclin D, cdk2, cdk4) in rats (n = 6; control rats, n = 5) subjected to transient (2 h) middle cerebral artery occlusion (MCAo) and 46 h of reperfusion. Few apoptotic cells were detected in the non-ischemic hemisphere of control rats. In ischemic animals, scattered apoptotic cells were present in the ischemic core and clustered apoptotic cells were present and localized to the inner boundary zone of the ischemic core. Proteins were preferentially localized to the cellular cytoplasm of control rats and in the non-ischemic hemisphere of rats subjected to MCAo. However, after MCAo these proteins were expressed and were preferentially localized to nuclei within the ischemic lesion. DNA damage induced proteins (wt-p53 and p53-response proteins) were preferentially expressed within apoptotic cells after ischemia. DNA repair proteins and cell cycle proteins were preferentially expressed within morphologically intact cells and in reversibly damaged cells in the ischemic areas. The selective expression of proteins associated with DNA damage, DNA repair and cell cycle observed in morphologically intact cells, ischemic injured cells and apoptotic cells suggests a differential role for these proteins in cell survival and apoptosis after stroke.

Animals↗

PubMed1997

Neuropeptide amidation in Drosophila: separate genes encode the two enzymes catalyzing amidation.

In vertebrates, the two-step peptide alpha-amidation reaction is catalyzed sequentially by two enzymatic activities contained within one bifunctional enzyme called PAM (peptidylglycine alpha-amidating mono-oxygenase). Drosophila head extracts contained both of these PAM-related enzyme activities: a mono-oxygenase (PHM) and a lyase (PAL). However, no bifunctional PAM protein was detected. We identified cDNAs encoding an active mono-oxygenase that is highly homologous to mammalian PHM. PHM-like immunoreactivity was found within diverse larval tissues, including the CNS, endocrine glands, and gut epithelium. Northern and Western blot analyses demonstrate RNA and protein species corresponding to the cloned PHM, but not to a bifunctional PAM, leading us to predict the existence of separate PHM and PAL genes in Drosophila. The Drosophila PHM gene displays an organization of exons that is highly similar to the PHM-encoding portion of the rat PAM gene. Genetic analysis was consistent with the prediction of separate PHM and PAL gene functions in Drosophila: a P element insertion line containing a transposon within the PHM transcription unit displayed strikingly lower PHM enzyme levels, whereas PAL levels were increased slightly. The lethal phenotype displayed by the dPHM P element insertion indicates a widespread essential function. Reversion analysis indicated that the lethality associated with the insertion chromosome likely is attributable to the P element insertion. These combined data indicate a fundamental evolutionary divergence in the genes coding for critical neurotransmitter biosynthetic enzymes: in Drosophila, the two enzyme activities of PAM are encoded by separate genes.

Amides↗

PubMed1997

Adenosine kinase inhibition protects brain against transient focal ischemia in rats.

Endogenous adenosine released locally during cerebral ischemia is neuroprotective, and agents which decrease adenosine inactivation may potentiate its protective effects. The effects of 5'-deoxy-5-iodotubercidin (5'd-5IT), an inhibitor of the adenosine-catabolizing enzyme, adenosine kinase, were studied in male Wistar rats subjected to 2 h of transient middle cerebral artery occlusion. 5'd-5IT or the vehicle (10% DMSO in saline) was administered i.p. 30 min before, and 2 h and 6 h after the induction of middle cerebral artery occlusion. The infarct volume was determine using 2,3,5-triphenyltetrazolium chloride staining 48 h after middle cerebral artery occlusion. The infarct volume was significantly reduced in rats treated with 1.85 mg/kg x 3 (57% reduction, P < 0.001) or 1.0 mg/kg x 3 (34% reduction, P < 0.05), but not 0.3 mg/kg x 3 5'd-5IT compared to vehicle-treated rats. The reduction of infarct volume was accompanied by a significant improvement in behavioral measures of neurological deficit. These data further support a role of adenosine in neuroprotection and suggest that adenosine kinase inhibition may be a useful approach to the treatment of focal cerebral ischemia.

Adenosine Kinase↗

PubMed1997

Immunoreactivity of cyclin D1/cdk4 in neurons and oligodendrocytes after focal cerebral ischemia in rat.

We investigated the expression of cyclin D1 and its kinase, cdk4, after induction of focal cerebral ischemia in the rat. Brain from rats (n = 6) subjected to 2 hours of transient middle cerebral artery occlusion and 46 hours of reperfusion, and control sham-operated (n = 3) and normal (n = 2) rats were processed for dual label immunohistochemical study for cellular identification of the expression of these cell cycle proteins. Antibodies raised against microtubule-associated protein 2 and neuronal specific enolase for neurons, glial fibrillary acidic protein for astrocytes, myelin basic protein for oligodendrocytes and lectin histochemical study with the B4-isolectin for microglia were used for cell type identification. Double staining for DNA fragmentation detection (TUNEL) and expression of cyclin D1 and cdk4 also was performed. Cyclin D1 and cdk4 were selectively expressed in morphologically intact or altered neurons and oligodendrocytes localized to the ischemic tissue. Apoptotic cells were not immunoreactive to cyclin D1 and cdk4 at 46 hours after 2 hours of middle cerebral artery occlusion. The selective expression of cell cycle proteins observed in nonapoptotic ischemic postmitotic neurons and oligodendrocytes suggests a role for these proteins in cell survival after transient focal cerebral ischemia.

Animals↗

PubMed1997

[Immunogenecity of expressed protein p68 from recombinant plasmid rpDJt in L. interrogans serovar lai].

There are two types of infection caused by pathogenic microorganisms, intracellular infection and intercellular infection. Infection of pathogenic leptospira is an intercellular infection. The immunological reaction of host to intercellular infection is unique. The potential immunogen of an expressed protein should meet three criteria: it can be degraded (by antigen-present cells in the host); it should have antigenic epitope which can be recognized by specific antibodies and have at least one epitope that can be recognized by an MHC II protein and T cell receptor. In this study we report the cloning of an L. interrogans protein in plasmid rpDJt and the immunogencity of the expressed protein derivative. A genomic library of L. interrogans serovar lai strain 017 was constructed with the plasmid vector pUC18. Recombinant plasmids, designated pDJH2 and pDJ8 were screened from the bank. EcoRI-inserted fragment of 1. 9 kb recombinant DNA of pDJH2 was ligated into T7 RNA polymerase/promoter vectors (pT7-7). Then they were transformed into E. coli JM109 (De3), one of subclones, designated rpDJt was achieved. SDS-PAGE showed that the molecular weights of expression proteins were 68 kd and 23 kd respectively, designated p68 and p23. Purifying and isolating p68 and p23, we separated them from SDS-Polyacrylamide gels by using Side-Strip method. After fragmenting and electroeluting, p68 and p23 were injected into guinea pigs and rabbits. An extremely strong immune response to p68 was obtained since an anti-p68 antibody response could be detected to a dilution 1:524,288 (guinea pigs) and 1:262,144 (rabbits) by ELISA while anti-P23 antibody being 1:1024 (the same to guinea pigs and rabbits). The results of improved MTT and conA 3HTdR transformation methods showed the activities and proliferation of Th-cells were increased in guinea pigs after p68 immunization (IL-6, 83.25 IU/ml, IL-2, 28.75 IU/ml; RPI, 2.04, SI, 65.62%) Thlymphocyte existed in two subclasses, the Th1- and Th2-cells. A major role of Th2-cells is to "help" B-cells differentiate, replicate, and secrete antibody. The properties of these interactions explain why p68 makes good antigen and p23 does not. The antigens responsible for eliciting the production of protective antibodies are not known; however, several outer membrane proteins on L. interrogans are candidates for vaccine. Our results suggest that expresion protein p68 from recombinants (rpDJt) may be a candidate for gene engineered subunit vaccine for Leptospirosis.

Animals↗

PubMed1997

[A rapid method for diagnosing alpha-thalassemia-1 of Southeast Asia type].

OBJECTIVE: To explore a rapid method for diagnosing alpha-thalassemia-1 of Southeast Asia type. METHODS: Seventy-six patients were detected by polymerase chain reaction (PCR). RESULTS: Thirty-one patients were diagnosed as alpha-thalassemia-1 of Southeast Asia type. PCR was compared with polyacrylamide gel electropheresis for detecting zeta-globin chain in 56 patients and the correspondance rate was 83.93%. Ten cases of prenatal diagnosis were performed by PCR, and the results showed that one was Hb bart's hydrop fetalis, four were carriers of alpha-thalassemia-1 of Southeast Asia type, and the others were normal fetalis or carrier of alpha-thalassemia-2. CONCLUSION: The PCR method is simple and accurate for diagnosing alpha-thalassemia of Southeast Asia type, and it provides a new approach to the prenatal diagnosis of alpha-thalassemia fetalis and the detection of alpha-globin gene cluster.

Adolescent↗

PubMed1996

Progesterone is neuroprotective after transient middle cerebral artery occlusion in male rats.

Progesterone (PROG) is a neurosteroid, possessing a variety of functions in the central nervous system. Exogenous PROG has been shown to reduce secondary neuronal loss in conjunction with attenuated brain edema after cerebral contusion and to reduce brain edema after focal cerebral ischemia. In the present study, we assessed the neuroprotective potential of PROG in a model of focal cerebral ischemia in the rat. Forty-eight male Wistar rats were randomly assigned to 4 groups, i.e. pretreatment with water soluble PROG, or dimethyl sulfoxide (DMSO) dissolved PROG, or DMSO as control or delayed treatment with DMSO dissolved PROG. Middle cerebral artery occlusion (MCAO) was induced by insertion of an intraluminal suture and reperfusion was performed by withdrawing the suture. Pretreatments were initiated 30 min before MCAO via intraperitoneal injection. Delayed treatment was initiated upon reperfusion following 2 h of MCAO. Infarct volume, body weight loss, and neurological deficit were measured 48 h after MCAO. Pre- and delayed treatment with DMSO dissolved PROG resulted in a 39% (P < 0.05) and 34% (P < 0.05) reduction in cerebral infarction, respectively, along with decreased body weight loss and improved neurological function as compared to control animals, whereas no statistically significant reduction in infarct volume by water soluble PROG was found. We demonstrated that administration of PROG to the male rat before or 2 hours after onset of MCAO reduces ischemic cell damage and improves physiological and neurological function 2 days after stroke. These results suggests potential therapeutic properties of PROG in the management of stroke.

Animals↗