Biomedical subjects

Wen-Bin Li

Publications and source records attributed to Wen-Bin Li.

At least 19 recordsLinked to original sources

PubMed2007

The upregulation of glial glutamate transporter-1 participates in the induction of brain ischemic tolerance in rats.

Glial glutamate transporter-1 (GLT-1) plays an essential role in removing glutamate from the extracellular space and maintaining the glutamate below neurotoxic level in the brain. To explore whether GLT-1 plays a role in the acquisition of brain ischemic tolerance (BIT) induced by cerebral ischemic preconditioning (CIP), the present study was undertaken to observe in vivo changes in the expression of GLT-1 and glial fibrillary acidic protein (GFAP) in the CA1 hippocampus during the induction of BIT, and the effect of dihydrokainate (DHK), an inhibitor of GLT-1, on the acquisition of BIT in rats. Immunohistochemistry for GFAP showed that the processes of astrocytes were prolonged after a CIP 2 days before the lethal ischemic insult, which could protect pyramidal neurons in the CA1 hippocampus against delayed neuronal death induced normally by lethal ischemic insult. The prolonged processes extended into the area between the pyramidal neurons and tightly surrounded them. These changes made the pyramidal layer look like a 'shape grid'. Simultaneously, the prolonged and extended processes showed a great deal of GLT-1. Western blotting analysis showed significant upregulation of GLT-1 expression after the CIP, especially when it was administered 2 days before the subsequent lethal ischemic insult. Neuropathological evaluation by thionin staining showed that DHK dose-dependently blocked the protective role of CIP against delayed neuronal death induced normally by lethal brain ischemia. It might be concluded that the surrounding of pyramidal neurons by astrocytes and upregulation of GLT-1 induced by CIP played an important role in the acquisition of the BIT induced by CIP.

Animals↗

PubMed2006

Optical oscillator strengths for valence-shell and Br-3d inner-shell excitations of HCl and HBr.

Absolute optical oscillator strength density spectra for valence-shell excitations of HCl and HBr, as well as for Br-3d inner-shell excitations of HBr, have been determined by high-resolution electron-energy-loss-spectroscopy method in the dipole limit. Absolute optical oscillator strengths for the discrete transitions of HCl and HBr are reported and compared with the previous results determined by the photoabsorption method.

Journal Article↗

PubMed2006

Nitric oxide participates in the induction of brain ischemic tolerance via activating ERK1/2 signaling pathways.

The present study was undertaken to observe in vivo changes of expression and phosphorylation of ERK1/2 proteins during brain ischemic preconditioning and effects of inhibiting generation of nitric oxide (NO) on the changes to determine the role of ERKs in the involvement of NO participating in the acquired tolerance. Fifty-five Wistar rats were used. Brain ischemic preconditioning was performed with four-vessel occlusion for 3 min. Total ERK1/2 proteins and phospho-ERK1/2 in the CA1 hippocampus were assayed with Western immunoblot. Total ERK1/2 proteins did not change in period from 5 min to 5 days of reperfusion after preconditioning stimulus. While the level of phospho-ERK1/2 increased obviously to 223, 237, 300, 385 and 254% of sham level at times of 5 min, 2 h, 1, 3 and 5 days after preconditioning stimulus, respectively (P < 0.01). Administration of L-NAME, an inhibitor of NO synthase, 30 min prior to preconditioning stimulus failed to induce change in total ERK1/2 proteins (P > 0.05). However, phospho-ERK1/2 increased only to 138 and 176% of sham level at 2 h and 3 days after preconditioning stimulus, respectively, when animals were pretreated with L-NAME. The magnitudes of the increase were obviously low compared with those (237 and 385%) in animals untreated with L-NAME at corresponding time points (P < 0.01), which indicated that phosphorylation of ERK1/2 normally induced by preconditioning stimulus was blocked apparently by administration of L-NAME. The results suggested that phosphorylation of ERK1/2, rather than synthesis of ERK1/2 proteins, was promoted in brain ischemic preconditioning, and that the promotion was partly mediated by NO signal pathway.

Adaptation, Physiological↗

PubMed2006

Limb ischemic preconditioning induces brain ischemic tolerance via p38 MAPK.

It has been reported that limb ischemic preconditioning (LIP) could induce brain ischemic tolerance. In the present study, we investigated the role of p38 MAPK in the induction of brain ischemic tolerance by observing expression of phosphorylated p38 (p-p38) MAPK in the hippocampus after LIP and the effect of p38 MAPK inhibitor SB 203580 on the protection of LIP against delayed neuronal death (DND) in the CA1 hippocampus induced normally by brain ischemic insult. The results of Flow cytometry and Western blotting showed that expression of p-p38 MAPK initially increased at 6 h after LIP compared with sham group in the CA1 hippocampus. The increases reached peak at 12 h and lasted to 24 h after LIP. Expression of p-p38 MAPK was also increased in the CA3/dentate gyrus (DG) regions after LIP, but the beginning and peaking times were 1 and 3 days after LIP, which were relatively later than those in the CA1. Histological evaluation showed that LIP protected the CA1 hippocampal pyramidal neurons against DND induced by global brain ischemic insult for 8 min, suggesting the occurrence of brain ischemic tolerance. Pretreatment with SB 203580 at 30 min before LIP effectively blocked the ischemic tolerance induced by LIP. Together, it could be concluded that activation of p38 MAPK played an important role in the brain ischemic tolerance induced by LIP, and that components of the p38 MAPK cascade might be targets to modify neuronal survival in ischemic tolerance.

Analysis of Variance↗

PubMed2006

The role of extracellular signal-regulated kinases in the neuroprotection of limb ischemic preconditioning.

To clarify the role of phosphorylated extracellular signal-regulated kinases (pERK1/2) in the neuroprotection of limb ischemic preconditioning (LIP) in rats, we investigated the expression of pERK1/2 using Western blot and flow cytometry in the hippocampus after LIP and the effect of pERK1/2 inhibitor PD 98059 on the neuroprotection of LIP against delayed neuronal death (DND) in the CA1 hippocampus normally induced by severe ischemic insult. It demonstrated that pERK1/2 in the hippocampus increased after LIP. In the CA1 hippocampus, ERK1/2 activation began to increase at 6h and reached peak at 12h after LIP, and decreased to sham level at 5d after LIP. On the other hand, in the CA3/DG, pERK1/2 enhanced at 1d, reached peak at 3d, and lasted to 5d after LIP. Pretreatment with PD 98059 before LIP blocked the neuroprotection of LIP in a dose-dependent manner. These findings supported that the upregulation of pERK1/2 in the CA1 hippocampus contributed to the neuroprotection of LIP against DND normally caused by the brain ischemic insult.

Animals↗

PubMed2006

Developmental genetic analysis of seed size in soybean (Glycine max).

Seed size is one of the important factors of soybean [Glycine max (L.) Merrill] yield. There have been lots of reports about genetic effects and physiology--ecological researches on seed size, but the genetic behaviors of genes during seeds development were rarely discussed. Analysis of main genetic effects for fresh seed size (FSS) and dry seed size (DSS) of soybean was conducted with diallel cross data by using a seed genetic model. Analyses of unconditional and conditional variances and correlations were used to evaluate the developmental behavior of soybean. The phenotypic means of FSS and DSS in soybean at eight stages among three generations reached the highest value at 9/6 and 9/13, respectively. The means of FSS decreased dramatically after 9/6, but the means of DSS maintained relatively stable tendency at corresponding periods. The unconditional variance analysis showed that FSS and DSS were controlled by embryo, cytoplasmic and maternal effects in the whole growth period. Genetic effects due to cytoplasmic and maternal effects were relatively important for FSS and DSS at most of the growth periods. Conditional variance analysis showed that genes from different genetic system expressed discontinuously in the whole growth period. The net genetic effects due to cytoplasmic and maternal plant on FSS and DSS were larger than those of embryo effects at most of the growth periods. Different genetic system can affect the relationship of various stages to mature solely or simultaneously. Embryo additive effects at 8/16, embryo dominance effects at 8/9 and 8/16, maternal plant dominance effects at 8/2 and 8/16 could ultimately affect the performance of FSS at maturing stage. Embryo additive effects at 8/2 and 9/13, cytoplasm effects at 8/9, maternal plant dominance effects at 8/2 could ultimately affect the performance of DSS.

Analysis of Variance↗

PubMed2006

Gastrotracheal and gastrobronchial fistulas: management with covered expandable metallic stents.

PURPOSE: The present study evaluated the clinical results of covered tracheobronchial metallic stent placement in the management of gastrotracheal fistulas (GTFs) and gastrobronchial fistulas (GBFs). MATERIALS AND METHODS: Sixteen patients with GTFs or GBFs after esophagogastrectomy were treated with one of two types of covered tracheobronchial metallic stents: a hinged stent or a straight stent. These included 12 GTFs and four GBFs. Thirteen hinged stents and three straight stents were placed during the initial procedure. Data regarding the technical success of stent placement, initial clinical success and failure, fistula reopening, and complications were obtained. RESULTS: Stent placement was technically successful in all patients. The stent completely sealed off the fistula in 12 of 16 patients (75% initial clinical success rate), whereas the remaining four patients (25%) had persistent aspiration symptoms as a result of incomplete GTF or GBF closure (ie, initial clinical failure). During follow-up, the fistula reopened in three of the 12 patients in whom initial clinical success was achieved (25%). Two reopened fistulas were sealed off with stent placement, and one was treated with a nasoenteric feeding tube and a nasogastric decompression tube. All patients died during the 1-year follow-up period; mean survival time was 17 +/- 3.02 weeks (range, 1-42 weeks) after stent placement. Mean survival in patients in whom initial clinical success was achieved was significantly longer than in patients with initial clinical failure (P = .003; log-rank test). CONCLUSION: Use of covered metallic stents appears to be a safe and moderately effective procedure to occlude GTFs and GBFs.

Adult↗

PubMed2006

[The effect of hyperoxia on transdifferentiation of type II alveolar epithelial cells in premature delivery rat].

AIM: To investigate the effect of hyperoxia on the transdifferentiation of type II alveolar epithelial cells (AECII) in premature delivery rats. METHODS: AECII from fetal rat lung were cultured primarily to establish a model of cells damaged by hyperoxia. The morphological changes of the cells were observed by inverted phase contrast microscope and transmission electron microscope. AECII-specific surfactant protein C (SP-C) and AECI-specific aquaporin 5 (AQP5) were detected by immunocytochemical staining. The expression levels of SP-C, AQP5 mRNAs and their protein were detected by RT-PCR and flow cytometry. RESULTS: With the time of exposure to hyperoxia, primarily cultured AECII spread and flattened, losing lamellar bodies and microvilli. They rapidly lost their characteristics and gained some AECI appearance. With their morphological changes, AECII stopped expressing AECII-specific protein SP-C but began expressing AECI-associated protein AQP5. Compared with exposure to air at the same time in air group for 24, 48 and 72 hours, the expression rate of SP-C mRNA in positive cells and fluorescence index (FI) decreased markedly in 3 groups, but compared with exposure to air for 24 and 48 hours the expression of AQP5 increased significantly in 2 groups. The expression of AQP5 began decreasing and showed no marked difference compared with air group at the same time of for 72 hours. CONCLUSION: The transdifferentiation of AECII induced by hyperoxia may play a key role in the repair of alveolar epithelial cell injury in premature delivery rats.

Animals↗

PubMed2005

[Construction and primary analysis of subtractive library induced by soybean mosaic virus (SMV)].

SMV is one of main diseases of soybean, which could affect yields and quality of soybean seriously. It was effective to soybean breeding by studying the expression of resistant gene to SMV with molecular technology. In this study, a soybean resistance line, DongNong 8143, was used to construct a subtractive cDNA library by SSH from soybean leaves inoculated by SMV No.1 at primary stage. cDNA dominantly or specifically expressed in infected leaves was purified using PCR Purification Kit and cloned into pGEM-T easy vector. Colonies were grown on LB-agar plates containing ampicillin, X-gal and IPTG. A subtractive plasmid library was constructed by SSH. Then the library was transformed to host bacteria E. coli DH5alpha, and the titer of the library was measured as 2 x 10(3) . 64 clones were picked up randomly and sequenced. Of them there is 50 clones which result of sequenced were good. The length of EST fragment varied from 136bp to 691bp, and the average length is 456bp. Among them, 41 sequences has poly(A). Through ESTs were compared with sequences in unigene database of GeneBank with BLASTn and BLASTx algorithm, 38 ESTs of them had comparatively clear results and the percent of them in acquired ESTs is 74%. The EST expression profile showed that the resistance-related genes include cell protection, signal transduction, restrict pathogen growth, system acquired resistance, and house-keeping gene. There are 12 ESTs, which have not comparatively clear results, that maybe new genes.

Expressed Sequence Tags↗

PubMed2004

Limb ischemic preconditioning attenuates apoptosis of pyramidal neurons in the CA1 hippocampus induced by cerebral ischemia-reperfusion in rats.

The purpose of this study was to investigate the effects of limb ischemic preconditioning (LIP) on apoptosis of pyramidal neurons in the CA1 hippocampus induced by global cerebral ischemia-reperfusion in rats. Forty-six rats whose bilateral vertebral arteries were occluded permanently were assigned to one of four groups: sham group, limb ischemia group, cerebral ischemia group and LIP group. LIP was performed by occluding the bilateral femoral arteries for 10 min 3 times in an interval of 10 min. Global cerebral ischemia was underwent by occluding the bilateral common carotid arteries for 8 min immediately after LIP. Assays for apoptosis of the hippocampal neurons were biologically and morphologically performed using gel electrophoresis, TUNEL and AO/EB staining. Characteristic DNA ladder was clearly visualized with gel electrophoresis in the hippocampus in cerebral ischemia group, but not in LIP group. The number of TUNEL-positive cells in the CA1 hippocampus was significantly reduced by LIP from 69.8+/-12 (cerebral ischemia group) to 17.8+/-5.8 (P<0.01). AO/EB staining also showed a reduction of apoptosis in LIP group compared with cerebral ischemia group. These results suggest that LIP can inhibit hippocampal neuronal apoptosis induced by cerebral ischemia-reperfusion, which contributes to the protection against the delayed neuronal death induced by cerebral ischemic insult.

Animals↗

PubMed2004

[MK-801 inhibits formalin-induced cyclooxygenase-2 expression in the dorsal horn of the spinal cord in rats].

To investigate the effect of N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 on the formalin-induced cyclooxygenase-2 (COX-2) expression in the dorsal horn of the rat spinal cord. Forty-eight male Sprague-Dawley rats were divided into 4 groups: control, formalin, formalin+normal saline (NS) and formalin+MK-801 groups. Rats in formalin, formalin+NS and formalin+MK-801 groups were subcutaneously injected with 0.2 ml 5% formalin into the plantar surface of the right hind paw. NS or MK-801 solution (10 microl) was intrathecally injected under transient ether anesthesia 15 min prior to the formalin injection in the formalin+NS and formalin+MK-801 groups, respectively. Flinch reflex was measured within 1 h after the formalin injection and expression of COX-2 in the dorsal horn of the L(5) segment of the spinal cord was assayed 24 h after the formalin injection using immunohistochemistry. Formalin evoked a biphasic flinch reflex. MK-801 produced a limited effect on the flinch reflex of phase 1, but produced significant and dose-dependent suppression on the flinch reflex of phase 2. The number and immunostaining density, shown by grey degree which was inversely proportional to the immunostaining density, of immunoreactive soma in the superficial (mainly I-II) and deep (IV-VI) laminae of the L(5) spinal cord in formalin and formalin+NS groups increased significantly, in contrast to those in the control group (p<0.01). The number and immunostaining density of immunoreactive soma decreased significantly in formalin+MK-801 group, in comparison with the formalin+NS group (p<0.05). The degree of the decrease was proportional to the dosage of MK-801 used. In addition, there were some immunoreactive processes especially in the superficial laminae, which extended as a continuous band across the dorsal horn after the formalin injection. Change in immunostaining density of the processes after administration of MK-801 was similar to that in the immunoreactive soma. The results showed that intrathecal injection of MK-801 significantly inhibited the increase of COX-2 expression in the spinal dorsal horn induced by the formalin injection in a dose-dependent manner, suggesting that the activation of NMDA receptor is one of the mechanisms for the formalin-induced increase of COX-2 expression in the spinal dorsal horn.

Animals↗

PubMed2004

A short cerebral ischemic preconditioning up-regulates adenosine receptors in the hippocampal CA1 region of rats.

Pharmacologically blocking or stimulating studies have showed the crucial role of adenosine receptors in the protective effect of cerebral ischemic preconditioning (CIP). However, little is know about whether the adenosine receptors are up-regulated in the process. In the present study, changes in expression of adenosine receptors in the CA1 hippocampus after a short CIP in a period of 3 min were investigated in rat four-vessel occluding (4VO) brain ischemic model using immunohistochemistry. The experiments were performed on groups of sham, 4 h, 1, 3, and 7 days (n = 6 in each group) after the CIP. The number and immunostaining density of immunoreactive cells for A1 and A2b adenosine receptors in the CA1 hippocampus were significantly increased after the CIP. For A1 adenosine receptor, the increase occurred in CA1 pyramidal neurons. While for A2b adenosine receptor, the increase occurred in the stratum radiatum of the CA1. The immunoreactive cells for A2b receptor showed distinct morphological characteristics of astrocytes. The increases were consistent in time course (1-7 days) with the development of the ischemic tolerance induced by the CIP. It was concluded that up-regulation of adenosine receptors may also play an important role in the protective effect of CIP.

Animals↗

PubMed2004

[Genetic diversity analysis of brown cotton and green cotton].

Genetic diversity analysis of brown cotton Xincai 1 and Xincai 2 and green cotton Xincai 3 and Xincai 4 and other 47 color cottons was conducted by the random amplified polymorphism DNA (RAPD) techniques, using 6 random primers. Cluster and similarity analysis of these cottons showed that the differences in genetic relationship and similarity among the brown cottons, green cottons and brown-green cottons are not remarkable. The results also reflect that the genetic bases of the brown and green cottons are narrow, and they are at the same genetic diversity level. These results are probably due to the same basic germplasms, the same breeding aims and the similar breeding approaches.

Cluster Analysis↗

PubMed2003

[Intrathecal injection of Sar9, Met(O2)11-substance P, neurokinin-1 receptor agonist, increases nitric oxide synthase expression and nitric oxide production in the rat spinal cord].

In the spinal cord, nitric oxide (NO) pathway is involved in pain and hyperalgesia, and nitric oxide synthase (NOS) expression and NO production are upregulated following several noxious and lesion stimuli. However, the mechanism of the increases is yet not well understood. The present study was designed to address the question of whether substance P (SP) released in the spinal cord enhances NOS expression and NO production of the spinal cord in rats. [Sar(9), Met(O2)(11)]-substance P (Sar-SP), a neurokinin-1 (NK-1) receptor agonist, was administered by intrathecal injection via L(5)-L(6) intervertebral space to induce nociception. The pain threshold was determined by hot water induced tail flick test. NOS expression of the L(5) segment of the spinal cord was determined using NADPH-d histochemical staining. NO production of the lumbar enlargement of the spinal cord was determined by assaying NO3(-) and NO2(-), the end product of NO metabolism, using the method of aqua fortis reduction. We found that (1) intrathecal injection of Sar-SP (6.5 nmol) elicited a characteristic, caudally directed, nociceptive behavioural response consisting of intense biting, licking and scratching episodes. Tail flick test showed decrease in pain threshold. (2) following the behavioural responses, the NOS expression level, including the number and the staining density of the NADPH-d reactive cells, increased in the superficial portion of the dorsal horn (Laminae I-II) and the grey matter surrounding the central canal (LaminaX) of the L(5) segment of the spinal cord after the Sar-SP intrathecal injection. At the same time, NO production in the enlargement of the spinal cord increased. (3) The decreased pain threshold and the increases in NOS expression and NO production could be substantially inhibited by intrathecal injection of [[D-Arg(1), D-Trp(7,9), Leu(11)]-substance P] (spantide) (5 microg), a non-selective antagonist of NK-1 receptor, 5 min prior to the Sar-SP injection. It might be concluded that the release of SP resulted from nociceptive afferents increased NOS expression and NO production of the rat spinal cord.

Animals↗

PubMed2003

Distinct roles of Kv1 and Kv3 potassium channels at the calyx of Held presynaptic terminal.

Despite identification of >100 potassium channel subunits, relatively little is known about their roles in synaptic transmission. To address this issue we recorded presynaptic potassium currents (IPK) directly from the calyx of Held terminal in brainstem slices of rats. IPK was composed of a 4-aminopyridine (4-AP)-sensitive component and a smaller 4-AP-insensitive component composed of an iberiotoxin-sensitive current and an unidentified slowly activating potassium current. IPK could also be separated into a tetraethylammonium (TEA; 1 mm)-sensitive high-voltage-activated component and a margatoxin (10 nm)-sensitive low-voltage-activated component, which was also blocked by dendrotoxin-I (200 nm) and tityustoxin-Kalpha (100 nm). In outside-out patches excised from calyceal terminals, TEA (1 mm) consistently and to a large extent attenuated IPK, whereas margatoxin attenuated IPK only in a subset of patches (three of seven). Immunocytochemical examination using Kv subtype-specific antibodies indicated that multiple Kv1 and Kv3 subtypes were present at the calyceal terminal. In paired presynaptic and postsynaptic whole-cell recordings, TEA (1 mm) increased both the duration and peak amplitude of presynaptic action potentials and simultaneously potentiated EPSCs. Margatoxin alone had no such effect but reduced the amount of depolarization required for action potential generation, thereby inducing a burst of spikes when the nerve terminal was depolarized for a prolonged period. Thus, at the calyx of Held terminal, Kv3 channels directly regulate evoked transmitter release, whereas Kv1 channels reduce nerve terminal excitability, thereby preventing aberrant transmitter release. We conclude that both Kv3 and Kv1 channels contribute differentially to maintaining the fidelity of synaptic transmission at the calyx of Held.

4-Aminopyridine↗

PubMed2003

[Effects of alpha-methyl-(4-tetrazolyl-phenyl) glycine on the induction of hippocampal ischemic tolerance in the rat].

To explore the role of metabotropic glutamate receptor 2/3 mGluR 2/3 in the induction of brain ischemic tolerance (BIT), the influences of mGluR2/3 antagonist alpha-methyl-(4-tetrazolyl-phenyl) glycine (MTPG) on the induction of BIT and expression of glial fibrillary acidic protein (GFAP) in the hippocampus were observed using thionin staining and GFAP immunohistochemical staining in a rat brain ischemic model with four-vessel occlusion (4VO). Fifty-four rats, of which bilateral vertebral arteries were occluded permanently by electrocautery, were divided into 5 groups: (1) sham operated group (n=8): the bilateral carotid common arteries (BCCA) were separated, but the blood flow was not blocked; (2) ischemia group (n=8): the blood flow of BCCA was blocked for 8 min; (3) ischemic preconditioning (IP) group (n=8): the blood flow of BCCA was occluded for 3 min as a cerebral ischemic preconditioning (CIP), and then the rats were exposed to an 8-min brain ischemic insult 24 h after the CIP; (4) MTPG+IP group (n=22): MTPG was administered 20 min before the CIP, then the rats were exposed to an 8-min brain ischemia insult 24 h after the CIP. In order to examine dosage dependency in the effect of MTPG, 4 dosages of MTPG (0.4, 0.2, 0.04 and 0.008 mg) were administered; (5) MTPG+ischemia group (n=8): an ischemic insult for 8 min was given 24 h after the administration of MTPG (0.2 mg). MTPG was injected into the right lateral cerebral ventricle. The results obtained are as follows. (1) Ischemic insult for 8 min increased the histological grade (HG) and reduced the neuronal density (ND) significantly, and also increased the expression of GFAP significantly (P<0.05 vs sham-operated group). (2) In the IP group, the above changes were not observed, indicating that CIP could protect pyramidal neurons against the ischemic insult. (3) The protective effects of CIP were blocked by MTPG, as manifested by the significant increase in HG and decrease in ND in the MTPG+IP group (P<0.05 vs sham-operated group). The changes were dose-dependent. (4) No obvious difference in the HG, ND and expression of GFAP was detected between the groups of MTPG+ischemia and ischemia. The above results indicate that MTPG blocks the induction of BIT induced by CIP, suggesting that mGluR2/3 participates in the induction of BIT.

Alanine↗

PubMed2003

[Effect of nitric oxide synthase inhibitor L-NAME on the induction of brain ischemic tolerance in rats].

To explore the role of NO in the induction of brain ischemic tolerance (BIT) in vivo, the effect of nitric oxide synthase (NOS) inhibitor L-NAME on the induction of BIT induced by cerebral ischemic preconditioning (CIP) was investigated in the hippocampal CA1 subfield in CIP and ischemic insult models established by rat four-vessel occlusion using brain tissue section and thionine staining methods. Fifty-four male Wistar rats were divided into 6 groups: (1) sham-operated group (n=6): bilateral common arteries were separated without occluding the cerebral blood flow; (2) ischemia group (n=6): an ischemic insult for 10 min was given; (3) CIP+ischemia group (n=6): 3-min CIP was preformed 72 h prior to 10-min ischemic insult; (4) L-NAME group (total n=24, n=6 for each subgroup): L-NAME (5 mg/kg, i.p.) was administered 1 h prior to CIP and 1, 12 and 36 h after CIP, respectively. Other procedures were the same as those for the CIP+ischemia group; (5) L-NAME+L-Arg group (n=6): L-NAME (5 mg/kg, i.p.) and L-Arg (300 mg/kg, i.p.) were administered 1 h prior to CIP, other procedures were the same as those for the L-NAME group; (6) L-NAME+ischemia group (n=6): L-NAME (5 mg/kg, i.p.) was administered 72 h before the 10-min ischemic insult. The results showed that (1)10-min ischemic insult resulted in an increase in the histological grade (indicating a more serious tissue injury) and a decrease in pyramidal neuronal density (P<0.01); (2) the histological grade and neuronal density in hippocampal CA1 in the CIP+ischemia group were similar to those in the sham-operated group (P>0.05); (3) in the L-NAME group, administration of L-NAME brought about an increase in the histological grade and a decrease in neuronal density (P<0.01), suggesting that L-NAME blocked the protection of CIP; (4) the neuronal damage in L-NAME+L-Arg group was slighter than that in the L-NAME group, but still more serious than that in the CIP+ischemia group, suggesting that L-Arg partly reversed the blocking effect of L-NAME; (5) the morphological representations in L-NAME+ischemia group were basically similar to those in the ischemia group. The results mentioned above indicate that NO is involved in the induction of BIT in vivo. The blocking effect of L-NAME administered at 36 h after CIP was obviously weaker than the effects of L-NAME administered 1 h prior to CIP, and 1 or 12 h after CIP. It is suggested that NO is involved in the induction of BIT at an early stage and that the involvement might take place via activating cascades of the events.

Animals↗

PubMed2003

[Pituitary adenylate cyclase activating polypeptide protects neuro-2a cells from beta amyloid protein cytotoxicity by modulating intracellular calcium].

MTT analysis and intracellular calcium measurement by using confocal laser scanning microscopy were used to study the possible mechanism of protective effect of pituitary adenylate cyclase activating polypeptide 27 (PACAP27) from beta amyloid protein (Abeta)-induced neurotoxicity. The results showed that treatment with PACAP (less than 0.1 micromol/L) increased the survival and reproductive ability of neuro-2a cells and protected the neuro-2a cells from being injured by Abeta. The protective effect of PACAP27 was reversed by the competitive PACAP receptor antagonist PACAP6-27. An increase in intracellular calcium was observed when the cells were challenged with Abeta and PACAP. But the calcium increase induced by Abeta kept stable for a long time while PACAP caused a transient rise in intracellular calcium. The intracellular calcium increase induced by Abeta was blocked by pretreatment with PACAP for 10 min. It is suggested that the neuroprotective effect of PACAP against neuronal damage induced by Abeta may result from its role in inhibiting the sustained rise in intracellular calcium.

Amyloid beta-Peptides↗