Preconditioning with 3-nitropropionic acid induces rat cerebral ischemic tolerance and increases expression of glucose transporter 1 and glucose transporter 3

AIM: To explore the mechanism of 3-nitropropionic acid (3-NPA) preconditioning that induces cerebral ischemic tolerance in rats by affecting the expression of brain-type glucose transporters (GLUT1 and GLUT3) at mRNA and protein levels in cerebral tissues.METHODS: The male SD rats were used in the experiments and divided randomly into sham operation group (sham group, n=4), control group of 3-NPA preconditioning (3-NPA group, n=4), cerebral ischemia group (M group, n=16) and 3-NPA preconditioning group (IPC group, n=16). M group and IPC group were further divided into 4 subgroups according to the different reperfusion time(4 h, 12 h, 24 h and 48 h). All rats were killed at the corresponding time points. The cerebral tissues in the ischemic side (left) and coronal intermediate 1/3 of cortex were collected. The protein levels and mRNA expression of GLUT1 and GLUT3 were determined by Western blotting and RT-PCR. RESULTS: Compared with M group, the ischemic reperfusion and 3-NPA preconditioning induced the upregulation of GLUT1 and GLUT3 at protein levels with significant differences (F=5.848, P<0.05 and F=6.295, P<0.05, respectively), especially after ischemia-reperfusion for 48 h. The mRNA expression of GLUT1 in IPC group began to increase at 4 h, peaked at 48 h after reperfusion, with significant difference as compared to M group at the corresponding reperfusion time points in each group or sham group. In contrast, the mRNA expression of GLUT3 in IPC group increased at 24 h, and was the highest at 48 h as compared to cerebral ischemia group at the corresponding reperfusion time points or sham group.CONCLUSION: 3-NPA preconditioning increases the expression of GLUT1 and GLUT3 at protein and mRNA levels to maintain the energy supply in brain tissues, indicating a cerebral protective mechanism.     

Mechanisms underlying the protective effect of renal ischemic preconditioning on ischemia-reperfusion myocardium of rabbits

AIM: To investigate the mechanisms underlying the protective effect of kidney ischemic preconditioning on rabbit myocardium in case of ischemia-reperfusion and the possible role of oxygen free radicals in the process. METHODS: Animals were divided into four groups: ischemia/reperfusion(I/R), classical ischemic preconditioning(CIPC), kidney ischemic preconditioning (KIPC) and superoxide dismutase in combination with kidney ischemic preconditioning(SOD+KIPC). The endo genous myocardial pretective material, nitric oxide(NO) and 5'-nucleotidase(5'-NT) were checked in four groups. RESULTS: As compared with I/R group, both CIPC and KIPC could ameliorate left ventricular function, reduce plasma PLA₂ activity and arrhythogenic rate also, the myocardial 5'-NT and NO production were significantly higher than that of the rabbit of I/R group. However, the protective effect on rabbit myocardium was significantly weakened by the SOD administration before the ischemic preconditioning. CONCLUSION: Protective effect of KIPC on myocardium may be due to increase in endo genous myocardial protective materials, oxygen free radicals may play an important role in the endo genous myocardial protective material release.     

Dynamic changes of the concentration of nitric oxide in ischemic myocardium and its mechanism

AIM: The study was undertaken to explore the dynamic changes of the concentration of nitric oxide(NO) in ischemic myocardium and its mechanism.METHODS: In vivo myocardial ischemia of mice and in vitro perfused isolated heart of rat were used in the experiment. The effects of severity and time of ischemia on NO production, NOS activity and mRNA were examined, respectively. RESULTS: There was a considerable difference (P<0.01) in the concentration of NO between ischemia group [(9.12±1.40) μmol/L] and control group [(20.16±1.67) μmol/L] after Pit(30 U/kg) administration, and the concentration of NO of ischemic group significantly decreased [(9.17±1.33) μmol/L] compared with control group [(19.90±1.95) μmol/L] after 30 minutes of ischemia. Also, the concentration of NO after Pit(20 U/L) administration in K-H and 15 min of ischemia was (15.41±2.00) μmol/L and (15.09±2.00) μmol/L respectively in vitro, significantly lower than control group [(23.83±2.33) μmol/L and (23.63±2.52) μmol/L]. In addition, compared with control group, the number of NOS positive cells, NOS activity as well as mRNA expression in atrial muscle and ventricular muscle of ischemic group were markedly reduced, respectively. CONCLUSION: Myocardial ischemia could reduced the NO level in myocardium, down-regulation of NOS mRNA could be the possible mechanism.     

Time course and distribution of myocyte apoptosis induced by acute ischemia in rats

AIM:Myocyte apoptosis in rats can be induced by acute ischemia, but time course and distribution of myocyte apoptosis were unclear.METHODS:DNA agarose gel electrophoresis and TdT-mediated dUTP nick end-labling(TUNEL)assay were performed to evaluate apoptosis in mycardium exposed to 45 minutes, 2 hours, 6hours, 12 hours ischemia and sham-operated rats in vivo.RESULTS:DNA ladders were clearly visible in agarosegel of DNA from ischemic myocardium exposed to 2 hours, 6 hours and 12 hours ischemia, and DNA ladders became more apparent with increasing duration of ischemia.TUNEL positive cells with apoptotic morphologic characters were present in above ischemia time, and apoptotic index increased with increasing ischemia time.The majority of TUNEL positive cells were myocytes.Apoptotic index was higher in subendocardium than in subepicardium(P<0.101), while higher in border ischemia region than in the central ischemia area(P<0.105).CONCLUSION:A time-effect relation existed between the number of apoptosis and the time range of supposed time;Apoptotic myocytes scattered inthe ischemic myocardium, mainly localized at subendocardium and ischemic border.     

Effect of Xin-Tong capsule on nitric oxide production and cGMP content of ventricular myocardium in rats with experimental myocardial ischemia

AIM:To study the effect of xin-tong capsule on nitric oxide production and cGMP content of ventricular myocardium in rats with experimental myocardial ischemia. METHODS:Rat model of acute myocardial ischemia induced by pituitrin was used in this study, and the lift of ST segment in ECG was used as the index of myocardial ischemia. The NO₂^-/NO₃^- and cGMP contents of ventricular myocardium in rats with myocardial ischemia were determined.RESULTS: NO₂^-/NO₃^- and cGMP contents in ventricular myocardium of myocardial ischemia were (486±59) nmol/g protein and (0.38±0.08) nmol/g protein, respectively, and markedly lower than those of control (P＜0.01). After administration of Xin-Tong capsule, contents of NO₂^-/NO₃^- and cGMP in ventricular myocardium of rats with myocardial ischemia were obviously elevated . In comparison with control, ST segment of ECG in rats with myocardial ischemia was lifted, and the lift peak of ST segment occur in 45 min after myocardial ischemia (P＜0.01). Pretreatment of Xin-Tong capsule can improve conditions of myocardial ischemia . CONCLUSION:Xin-Tong capsule can elevate the contents of nitric oxide and cGMP, and attenuate myocardial ischemia injury in rats.     

Effects of ischemic preconditioning on oxidative stress and mitochondrial function in young and old rat myocardium with ischemia/reperfusion

AIM: To study the protective effect of ischemia preconditioning (IPC) on ischemia/reperfusion (IR)-damaged myocardium in young and old rats. METHODS: Male Wistar rats aged at 3 months (young) and 20 months (old) were used to establish myocardial IPC model and IR model with the method of Langendorff heart perfusion. The rats were divided into young ischemia/reperfusion (YIR) group, young ischemic preconditioning (YPC) group, old ischemia/reperfusion (OIR) group and old ischemic preconditioning (OPC) group. Transmission electron microscopy was used to observe the ultrastructural changes of myocardial tissue and myocardial mitochondria. The myocardial infarction area was determined by TTC staining. The lactate dehydrogenase (LDH) content in coronary effluent fluid and the levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in myocardial tissues were detected by the method of colorimetry. The levels of nitrated and carbonylated proteins in myocardial tissue were measured by ELISA. The myocardial cell apoptosis was analyzed by TUNEL assay. The mitochondrial respiratory function and mitochondrial permeability transition pore opening induced by calcium load were evaluated by oxygen electrode method. RESULTS: Compared with YIR group, the myocardial infarction area in YPC group was obviously smaller, SOD activity in myocardial tissues increased, LDH activity in coronary effluent fluid and the content of MDA decreased, and the levels of nitrated and carbonylated proteins in the cardiac tissues reduced. In YPC group, the mitochondrial membrane structure appeared intact, cristae of the mitochondria showed close arrangement, and the matrix was compressed under the electron microscope. Myocardial mitochondrial respiratory control rate, state Ⅲ oxygen consumption and the P/O ratio in YIR group all significantly increased, proton leak decreased, mitochondrial swelling induced by calcium distinctly reduced, and myocardial apoptosis rate declined. No significant difference of the above indexes between OIR group and OPC group was observed. Compared with YPC group, myocardial ultrastructural damage increased clearly, cardiac oxidative stress increased, mitochondrial respiratory function declined, and cell apoptosis and necrosis increased in OPC group. CONCLUSION: Ischemic preconditioning has protective effect against myocardial IR injury in young rat hearts, while old rat hearts were less sensitive to ischemic preconditioning, leading to bluntness of cardioprotection with IPC in aging hearts. This may be related to mitochondrial injury and severe cellular apoptosis caused by increase of cardiac oxidative stress levels in the aging ischemic preconditioning heart.     

Role of cAMP and cGMP in the regulation of bFGF gene expression of rat cardiomyocytes

AIM: To investigate the role of cAMP and cGMP in the regulation of bFGF gene expression of rat cardiomyocytes. METHODS: 8-Bromo-cAMP and sodium nitroprusside were added into the media to raise the concentrations of cAMP and cGMP of cultured cardiomyocytes, in situ hybridization and immunohistochemistry methods were used to identify the mRNA and protein expression of bFGF. The amount of bFGF mRNA and protein expression were detected by computor imaging analysis system MIAS exe. RESULTS: At 24 h after adding 8-Bromo-cAMP(0 1 mmol/L), bFGF mRNA and protein expression elevated significantly , at 48 h and 72 h it still expressed higher than that of control group( P< 0.05). But after adding sodium nitroprusside (1 mmol/L),bFGF expression decreased significantly,and especially at 48 h. CONCLUSION: The regulation of bFGF expression of cardiomyocytes is related to cAMP signal pathway.     

Effects of non-wounded ischemic preconditioning on ischemia-reperfusion injury in isolated rat hearts

AIM:To observe the protective effect of non-wounded ischemic preconditioning on ischemic/reperfusion injury in isolated rat hearts. METHODS: 25 male SD rats, weighting (250±30) g, were randomly divided into three groups: control group (C,n=8), anoxia/reoxygenation group (A,n=8) and non-wounded legs ischemic preconditioning group (N-WIP,n=9).Hearts were isolated from rats and perfused on a Langendorff apparatus with a normal Krebs-Henseleit buffer (saturation 95% O₂+5% CO₂) at a constant pressure (8.33 kPa) and temperature (37 ℃) in C group; Following 15 min equilibration, hearts were subjected to 15 min of global ischemia and 15 min reperfusion (37℃) in A group; Rats were subjected to non-wounded leg repeated-brief ischemic preconditioning, and then treated in procedure similar to A group in N-WIP group.The activities of superoxide dismutase (SOD) and Ca²⁺-Mg²⁺-ATPase, malondialdehyde (MDA) content of efflux from coronary vessel and myocardium, myocardium monophasic action potential and contractile force were measured before ischemia, 15 minutes after ischemia and 5, 15 minutes after reperfusion. RESULTS:Compared with A group, non-wounded legs ischemic preconditioning reduced the incidence of reperfusion arrhythmias (P＜0.05), decreased the content of MDA of myocardium (P＜0.01), enhanced the activities of SOD (P＜0.01) and stabilized myocardial membranous potential,the activity of Ca²⁺-Mg²⁺-ATPase and contractile function. CONCLUSION:These results indicate that non-wounded leg ischemic preconditioning has a protective effect on ischemia-reperfusion injury in isolated rat hearts. The mechanism may be related to the strength of antioxidation, the stability of Ca²⁺-Mg²⁺-ATPase activity and membranous structure in myocardium.     

Effects of ischemic preconditioning on cardiac myocyte apoptosis and expression of bcl-2 during myocardial ischemia/reperfusion in rats

AIM:To explore the effect of ischemic preconditioning on cardiac myocyte apoptosis and the expression of bcl-2 during myocardial ischemia/reperfusion in rats. METHODS:We use TUNEL,immunohistochemical and in situ hybridization(ISH) methods to detect the cardiac myocyte apoptosis and the expression of bcl-2 during myocardial ischemia/reperfusion in rats. RESULTS:①The numbers of positive cardiac myocyte nuclear and the percentage of positive cardiac myocyte nuclear in IP+I/R_3h group decreased significantly(P<0.05,P<0.01)compared with I/R_3h group,respectively.②The numbers of bcl-2 protein positive cardiomyocyte and the percentage of bcl-2 protein positive cardiomyocyte in IP+I/R_3h group were higher(P<0.01)than that of I/R_3h group,respectively.The numbers of positive bcl-2 mRNA cardiomyocyte and the percentage of positive bcl-2 mRNA cardiomyocyte in IP+I/R_1h group were higher(P<0.01)than that of I/R_1h group,respectively.CONCLUSION:① The first window of IP's protection could reduce cardiomyocyte apoptosis significantly.② Up-regulating the protein expression of bcl-2 in cardiomyocytes during I/R may be one of the mechanisms of first window of IP's protection.     

Study on protective mechanism of non-wounded ischemic preconditioning on rat ischemia/reperfusion myocardium

AIM:To investigate probable protective mechanism of non-wounded legs ischemic preconditioning on ischemia/reperfusion(I/R) myocardium. METHODS: 36 male SD rats, weighting (250±30) g,were divided into 4 groups.They are normal control(NC);I/R; classical ischemic preconditioning(C-IPC)and non-wounded legs ischemic preconditioning(N-WIPC). NO in plasm,expression of myocardial HSP 70 mRNA, the activities of 5’-NT and CAT of myocardium were observed in all groups. RESULTS:The level of NO in plasm significantly enhanced in groups C-IPC and N-WIPC compared with that in groups I/R and NC ( P <0.01),expression of myocardial HSP 70 mRNA was greatly increased in both C-IPC and N-WIPC groups, the activities of 5’-NT, CAT of myocardium were also raised in groups C-IPC and N-WIPC ( P< 0.05 vs I/R),but there was no difference between C-IPC and N-WIPC( P >0.05). CONCLUSION:The possible protective mechanism involved in N-WIPC is similar to that in C-IPC, which is due to increase of endogenous myocardial protective substances.     

An experimental exploration of focal inflammatory response in cerebral ischemic foci in the rat

AIM: To study the pathological relationship of vascular cell adhesion molecule-1 (VCAM-1) expression and monocyte/macrophage infiltration with focal brain ischemia. METHODS: Immunohistochemical technique and focal brain ischemia/reperfusion model were used in the study in order to explore profiles and time-course of VCAM-1 expression and monocyte macrophage (ED2 positive cell) infiltration in ischemic rat brain. RESULTS: VCAM-1 was up-regulated in microvascular endothelial cells in ischemic cortex at 1h postischemia, and continuously expressed during the time of reperfusion. ED2 positive cells infiltrated into ischemic cortex at 1h iscehmia/ 2h reperfusion and then ED2 positive cells increased gradually with the time of reperfusion, ED2 positive cell infiltration showed apparently relationship with VCAM-1 expression, and both of them exhibited the some changes of time-dependence. CONCLUSION: Cerebral ischemia induced VCAM-1 expression and ED2 positive cell infiltration and VCAM-1 may regulate the recruitment of ED2 positive cells in the ischemic brain region. The results suggested that VCAM-1 and ED2 positive cells may be participated in the pathogenesis of cerebral ischemic injury.     

Protein expression of cyclin D2 and p16 in proliferation and differentiation of cultured cardiac myocytes

AIM:To investigate the protein expression of cyclin D₂ and p16 in proliferation and differentiation of cultured cardiac myocytes.METHODS:One-day-old Sparague-Dawley rats were used. Cardiac myocytes(CM) were collected by a trypsin-dispersal method and cultured. Cell growth line and fluorescence activated cell sorting (FACS) were used to investigate the proliferation of CM. Ultra-thin sections were made to observe the ultrastructure of CM under transmission electron microscope. The expression of cyclin D₂ and p16 in CM were measured using immunocytochemistry and image analysis.RESULTS:①Results of cell growth line and FACS analysis showed that cultured CM could proliferate in the first 3 cultured days, but the ability decreased quickly, concomitant with differentiation. CM was obseved quiescent in cell cycle three days later. The ultrastructure of CM showed the large amount of myofilaments and mitochondrion. ②The protein expression of cyclin D₂ in 3,4,5 day CM group was 0.89 times(P＜0.05),0.80 times (P＜0.05) and 0.56 times (P＜0.01) of that in 1 day group, respectively. The expression of p16 in CM was increased during the culture process, 2,3,4,5 day group were 1.63 times, 1.72 times, 1.99 times and 2.84 times (P＜0.01) of that in 1 day group, respectively.CONCLUSION:Cultured neonatal rat cardiac myocytes could proliferate during the first 3 days after incubation, but the ability of proliferation decreased, from the fourth day, concomitant with differentiation. Cyclin D₂ and p16 play the key roles in CM postnatal development. Downregulation of cyclin D₂ and upregulation of p16 may induce CM differentiation.     

The expression of 53BP1 and 53BP2 gene in nasopharyngeal carcinoma

AIM:To investigate the expression map of two p53 binding proteins 53BP1 and 53BP2 in nasopharyngeal carcinoma (NPC) tissue. METHODS:The expression of 53BP1 and 53BP2 mRNA in NPC biopsy and control group are tested by RT-PCR. The expression of two mRNA in NPC paraffin section are examined by in situ hybridization. RESULTS:No expression of 53BP1 mRNA was found in NPC tissue and control group. However, expression of 53BP2 was detected in NPC biopsy and control group by RT-PCR, specific expressoin found cancerous nest in NPC paraffin section by in situ hybridization. CONCLUSION:The high expression of 53BP2 may be related to the development of NPC.     

The effect of glucose,lactate and pyruvate on the dynamic adaptation of cardiac mitochondrial oxygen consumption

AIM: To understand the effect of exogenous carbon substrate on the dynamic regulation of cardiac oxidative phosphorylation. METHODS: Method of mean response time measurement of the myocardial mitochondrial O₂ consumption (t_mito) was developed by van Beek. Glucose, lactate, or pyruvate as carbon substrate respectively for myocardial energy supply was perfused in isolated rabbit hearts with Tyrode solution at 37℃. RESULTS: When heart rate was stepped up from 120 to 140 and 220 (beat·min^-1) respectively the t_mito. We have measured was: (6.3±1.0)s and (7.4±0.9) s for glucose; (5.4±1.2) s and (7.0±0.9) s for lactate; (4.0±0.7)s and (6.5±0.6) s for pyruvate (two way ANOVA, P＜0.05, compared with lactate and glucose). CONCLUSION: The transport of reducing equivalent into the mitochondrial matrix might be a limitation factor of dynamic adaptation of cardiac mitochondrial oxidative phosphorylation during fast changes in ATP utilization.     

Effect of ischemia or hypoxia on vascular endothelial growth factor production in rat myocardium and its significance

AIM:To determine the relationship between ischemia, hypoxia and the production of vascular endothelial growth factor in rat myocardium and its basic mechanism. METHODS:(1) 28 Wistar rats were randomly divided into 4 groups: group A, normal control;group B, 1 day's acute myocardial infarction;group C, 3 day's acute myocardial infarction;group D, 7 day's acute myocardial infarction. (2) Rat cardiac myocytes cultured were primarily divided into some groups, hypoxia incubated 24 hours; PMA groups, hypoxia incubated 24 hours with PKC activator (PMA), A 0 ng/mL; B 10 ng/mL; C 100 ng/mL; D 1 000 ng/mL; Chelerythrine groups, hypoxia incubated 24 hours with PKC inhibitor (chelerythrine), A 0 nmol/L; B 10 nmol/L. (3) By computer scanned and quantitated, vascular endothelial growth factor (VEGF) protein was detected with immunohistochemical technique. RESULTS:The longer time of ischemia and hypoxia was, the higher the VEGF production.The relat ionship was found between the time of ischemia or hypoxia and the production of VEGF.The product ion of VEGF protein was further promoted by PMA with different concentrat ion, decreased by chelerythrine.CONCLUSION: Ischemia or hypoxia strongly stimulated the production of VEGF in myocardium, which played an important role in autoprotecting of ischemic or hypoxic myocardium. Hypoxia-induced PKC activation is one kind of basic mechanisms in this course.     

Effect of rosiglitazone on expressions of insulin receptor substrate-1 and glucose transporter 4 in skeletal muscle of type 2 diabetic rats with hyperlipemia

AIM: To investigate the effect of rosiglitazone on the expressions of insulin receptor substrate-1 (IRS-1) and glucose transporter 4 (GLUT4) in skeletal muscles of type 2 diabetic rats with hyperlipemia, and to explore the different pharmacological mechanism. METHODS: The model of type 2 diabetic rats with hyperlipemia was established by injecting low dosage of streptozotocin (STZ) and feeding with high fat diet. Then the diabetic rats were divided into two groups: untreated diabetic group and rosiglitazone-intervened diabetic group. The course of treatment lasted for 4 weeks. The expressions of IRS-1 and the GLUT4 proteins in the cell membrane of isolated rats skeletal muscles were detected by Western blotting. RESULTS: The fasting blood glucose, insulin and triglyceride contents in rosiglitazone-intervened diabetic group were lower than those in untreated diabetic group, but they were still higher than those in control group. The result of Western blotting showed that the expression of GLUT4 protein in rosiglitazone-intervened diabetic group was increased compared with untreated diabetic group, but its level was still lower than that in control group. The protein expression and tyrosine phosphorylation of IRS-1 in rosiglitazone-intervened diabetic group were significantly higher than those in untreated diabetic group and their levels were lower than those in control group. CONCLUSION: The effect of rosiglitazone on GLUT4 protein may link to its ability to induce the protein expression and tyrosine phosphorylation of IRS-1 in skeletal muscles in type 2 diabetic rats.     

Effects of norepinephrine preconditioning and ischemic preconditioning on apoptosis and Bcl-2, Bax expression in rat myocardial cells during myocardial ischemic reperfusion

AIM: To study the effects of norepinephrine preconditioning(NE-P) and ischemic preconditioning (IP)on apoptosis and Bcl-2, Bax expression in rat myocardial cells in myocardial ischemic reperfusion (I/R). METHODS: The model of rat ischemic-reperfusion was used to conduct NE-preconditioning. Apoptotic myocytes were detected with TUNEL. Bcl-2, Bax expression were detected with immunohistochemistry. RESULTS: The rate of apoptosis cells in I/R group was higher, the rate of apoptosis cells in NE-P group and IP was lower significantly than that in I/R group(P＜0.01). The expression of Bcl-2 in I/R group was lower, but the expression of Bax was higher, the expression of Bcl-2 in NE-P group was higher significantly than that in I/R group(P＜0.01), the expression of Bax in NE-P group was lower than that in I/R group(P＜0.01). There was no significantly difference between NE-P and IP group in the above parameters (P＞0.05). CONCLUSION: NE-P reduced myocyte apoptosis by I/R in rats; The expression of Bcl-2 ,Bax genes played an important role in myocardial apoptosis.     

Effect of Sini decoction on GST expression in the ischemic myocardium

AIM:To detect the effect of Sini decoction on glutathione S-transferase (GST) mRNA expression in the ischemic myocardium. METHODS:Kunming mice were randomly divided into control group, ischemic group and Sini decoction group. Total RNA was extracted from the myocardium of mice in each group. The effect of Sini decoction on the expression of GST gene was detected by RT-PCR. RESULTS:The expression of GST mRNA in Sini decoction group was significantly up-regulated compared with the ischemic group and control group.CONCLUSION:Sini decoction can promote the expression of GST gene,which may be related to its protective effect on ischemic myocardium.     

Effects of taurine on expression of glucose transporters in rat brain with diffused brain injury

AIM: To investigate the effect of taurine on the expression of glucose transporter 1 (GLUT1) and transporter 3 (GLUT3) in rat brain with diffused brain injury (DBI).METHODS: Sixty-four male Sprague-Dawley rats were randomly divided into 4 groups: sham-operated group, DBI group, low-dose taurine group (200 mg/kg, ig) and high-dose taurine group (300 mg/kg, ig).After fed with the corresponding drugs for 7 days, the animal model of DBI was made, and the rats were executed 24 h after DBI.The expression of GLUT1 and GLUT3 in the brain was detected by the methods of immunohistochemistry and Western blotting.The pathomorphological changes of the cerebral cortex were observed under electron microscope.RESULTS: The expression of GLUT1 was detected in capillary vascular endothelial cells in each group, and cytoplasm-positive cells or the cells with buffy membrane were observed.No significant difference of the GLUT1 expression in brain tissues between DBI group and sham-operated group was detected.Compared with DBI group, the expression of GLUT1 in the brain tissues were significantly increased in low-and high-dose taurine groups (P<0.01).The expression of GLUT1 in the brain tissues in low-dose taurine group were significantly higher than that in high-dose taurine group (P<0.05).The positive staining of GLUT3 only appeared in the periphery of the third ventricle in each group in the cells with buffy membrane or positive cytoplasm.The expression of GLUT3 in the brain tissues in DBI group was significantly higher than that in sham-operated group (P<0.01).The expression of GLUT3 in the brain tissues in low-and high-dose taurine groups was significantly higher than that in DBI group (P<0.01).Compared with low dose taurine group, the expression of GLUT3 in the brain tissues were significantly increased in high-dose taurine group (P<0.01).The pathological damage of cerebral cortex in low-dose taurine group was obviously alleviated.CONCLUSION: Taurine may take part in the neuroprotective mechanisms in DBI by increasing the expression of GLUT1 and GLUT3 at protein level to maintain the energy supply in brain tissues.