Effects of five-year intensive multifactorial intervention on the serum amyloid A and macroangiopathy in patients with short-duration type 2 diabetes mellitus / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>A five-year follow-up study of intensive multifactorial intervention was undertaken to assess the changes of circulating serum amyloid A (SAA) levels and the incidence of atherosclerosis (AS) in patients with short-duration type 2 diabetes mellitus (T2DM) without macroangiopathy, and whether intensive multifactorial intervention could prevent or at least postpone the occurrence of macroangiopathy.</p><p><b>METHODS</b>Among 150 patients with short-duration T2DM, 75 were assigned to receive conventional outpatient treatment (conventional group) and the others underwent intensive multifactorial integrated therapy targeting hyperglycemia, hypertension, dyslipidemia and received aspirin simultaneously (intensive group).</p><p><b>RESULTS</b>Plasma SAA levels were higher in diabetic patients than those in healthy control subjects, and decreased obviously after intensive multifactorial intervention. The levels of SAA were positively correlated with body mass index (BMI), waist hip ratio (WHR), triglyceride (TG), high sensitive C-reactive protein (hs-CRP) and common carotid intima-media thickness (CC-IMT). The standard-reaching rates of glycemia, blood pressure and lipidemia were significantly higher in intensive group than those of conventional group. The incidence of macroangiopathy decreased by 58.96% in intensive group compared with conventional group.</p><p><b>CONCLUSIONS</b>Intensive multifactorial intervention may significantly reduce the SAA levels and prevent the occurrence of AS in short-duration patients with T2DM. SAA might be one of the risk factors of T2DM combined with AS.</p>

Effects of Zibu Piyin recipe on SNK-SPAR pathway in neuron injury induced by glutamate / 中国结合医学杂志

<p><b>OBJECTIVE</b>To investigate the relationship between the excitotoxicity and serum-inducible kinase (SNK) and spine-associated Rap GTPase-activating protein (SPAR) pathway in primary hippocampal neuron injury induced by glutamate and furthermore, to explore the molecular mechanism of neuroprotection of Zibu Piyin Recipe (ZBPYR) and the relationship between ZBPYR and the morphological regulation of dendritic spines.</p><p><b>METHODS</b>The serum containing ZBPYR was prepared by seropharmacology. Reverse transcription and polymerase chain reaction (RT-PCR) was used to detect the expression of mRNA for SNK, SPAR, postsynaptic density protein 95 (PSD-95) and N-methyl-D-aspartate (NMDA) receptor subunits (NR1, NR2A and NR2B) in primary rat hippocampal neuron cultures after pretreatment with 10 micromol/L glutamate and ZBPYR serum.</p><p><b>RESULTS</b>ZBPYR serum pretreatment resulted in a significant down-regulation of glutamate-induced SNK mRNA expression (P<0.05). Significant up-regulation was seen on the mRNA expression of SPAR and PSD-95 (P<0.05). All these changes were dose-dependent. The mRNA expression of NR1, NR2A and NR2B was down-regulated to different degrees (P<0.05).</p><p><b>CONCLUSION</b>The mechanism of effect of ZBPYR on glutamate-induced excitotoxicity may be related to the regulation of SNK-SPAR signal pathway. ZBPYR may play a role in protecting and maintaining the normal morphology and structure of dendritic spines, which may be achieved by inhibiting the excessive activation of NMDA receptors.</p>

Association of SelS mRNA expression in omental adipose tissue with Homa-IR and serum amyloid A in patients with type 2 diabetes mellitus / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Tanis was reported as a putative receptor for serum amyloid A (SAA) involving glucose regulated protein in insulin regulated resistance. It was found to be dysregulated in diabetic rats (Psammomys obesus, Israeli sand rat) and its homologue for humans is SelS/AD-015. The present study analyzed mRNA expression of SelS in omental adipose tissue biopsies from patients with type 2 diabetes mellitus (T2DM), and age- and weight-matched nondiabetic patients, the relationship of SelS mRNA with Homa-IR and serum SAA level.</p><p><b>METHODS</b>Human omental adipose tissues from ten cases of type 2 diabetic patients and twelve cases of nondiabetic individuals were analyzed for the expression level of SelS mRNA by semiquantitative polymerase chain reaction (PCR), Homa-IR estimated by standard formula and SAA level by enzyme-linked immunosorbent assay (ELISA).</p><p><b>RESULTS</b>SelS mRNA expression, Homa-IR and serum SAA were higher in T2DM sufferers than in nondiabetic control group. SelS mRNA level was positively correlated with Homa-IR and SAA level in each group.</p><p><b>CONCLUSIONS</b>SelS protein may be involved in insulin resistance in Chinese with T2DM by acting as the SAA receptor, thus playing an important role in the development of T2DM and atherosclerosis.</p>

Effects of ginkgolide B against damage of cultured hippocampal neurons caused by glutamate / 中国应用生理学杂志

<p><b>AIM</b>To investigate protective effects of ginkgolide B (GB) in different administration modes on glutamate-induced neuronal damage.</p><p><b>METHODS</b>Essential GB were obtained by supercritical CO2 fluid extraction. Glutamate excitotoxicity were examined in primary cultures from neonatal Wistar rat, by using of Trypan blue dye staining, testing the lactate dehydrogenase leakage from cultured neurons and terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) method. The protective effects of GB in different administration modes (pre-treatment and post-treatment) were adopted and compared with the NMDA receptor uncompetitive antagonist-MK-801 in acute-treatment.</p><p><b>RESULTS</b>Treatment with GB in two administration modes both could increase ratio of surviving neuron, decrease LDH efflux and reduce ratio of neuron apoptosis in different degree, depended on dose in certain range. The protective effect of pre-treatment was superior to post-treatment, but inferior to MK-801.</p><p><b>CONCLUSION</b>GB can protect neurons against glutamate damage, and preventive using has more efficiency. The potential mechanism of its neural protection may be not only related to PAF receptor. If the predominant protection effect of GB in pretreatment is considered, precautionary intervention to high-risk population could have more value.</p>

The effect of simvastatin on the regeneration of sciatic nerve with crush injury in rats / 中国应用生理学杂志

<p><b>AIM</b>To explore the effect of Simvastatin on the regeneration of sciatic nerve with crush injury in rats.</p><p><b>METHODS</b>Animals were randomized into the following experimental groups: Simvastatin-treated, vehicle and sham-operated groups. Sciatic nerves with crush injury were performed. After surgery, the functional evaluation of nerve recovery, electrophysiologic assessment, histological assessment, serum IL-6 and lipid were performed.</p><p><b>RESULTS</b>The toe spread index of Simvastatin-treated rats after operation was higher significantly than vehicle rats at 5 d and 8 d (P<0.05). CMAP was higher and NCV was faster (P < 0.05). The serum IL-6 at 5 d of post-operation was significant lower (P < 0.05). Total serum cholesterol of Simvastatin-treated animals was higher than that of other animals (P < 0.05) at 2 weeks of post-operation. The histological analysis showed that the numbers of myelinated axons and the thickness of myelin sheath of Simvastatin-treated crush injury animals at 4 weeks of post-operation were more than that of vehicle animals.</p><p><b>CONCLUSION</b>The present study showed that Simvastatin could promote the regeneration of the sciatic nerve after crush injury in rats, partly through inhibiting immune and inflammatory responses and making the balance of serum cholesterol during these processes.</p>

Effects of ginkgo biloba extracts on NMDA-activated currents in acutely isolated rat hippocampal neurons / 中国应用生理学杂志

<p><b>AIM</b>To investigate effect of ginkgo biloba extract (GBE) on N-methyl-D-aspartate (NMDA)-activated currents (I(NMDA)) and evaluate further the modulatory effects of Micro-GBE/Nano-GBE.</p><p><b>METHODS</b>By means of whole-cell patch clamp technique, NMDA-activated currents from acutely isolated rat hippocampal neurons were recored.</p><p><b>RESULTS</b>The majority of the neurons examined (81.8%, 90/110) were sensitive to NMDA (1 mmol/L) and its co-agonist Gly (10 micromol/L). NMDA activated an inward current, which manifested apparent desensitization and could be blocked by its specific antagonist MK-801. After the neurons were treated with Micro/Nano GBE (0.1 mg/ml) followed by the application of NMDA (1 mmol/L) and Gly (10 micromol/L) for 30 s, it was show that NMDA-activated currents were obviously inhibited (P < 0.01, n = 8). The inhibitory rate were 40% +/- 17% and 64% +/- 15% respectively. It showed that the modulatory effect of Nano-GBE (dissolved in the stander extracellular solution) on NMDA-activated current was significantly higher than that of Micro-GBE (dissolved in DMSO) (P < 0.05).</p><p><b>CONCLUSION</b>The inward currents activated by NMDA could be depressed by Micro-GBE and Nano-GBE. The modulatory effects of GBE on NMDA-activated current are expected to contribute to the neuroprotective effects of ginkgo biloba extracts. In addition, at the same concentration, the modulatory effect of Nano-GBE on NMDA-activated current is better than that of Micro-GBE.</p>

Inhibitory effect of caffeine on GABA-activated current in acutely isolated rat dorsal root ganglion neurons / 生理学报

By means of whole-cell patch clamp technique, the modulatory effect of caffeine on GABA-activated currents (I(GABA)) was investigated in acutely isolated rat dorsal root ganglion (DRG) neurons. The majority of the neurons examined (113/116) were sensitive to GABA (1~1000 micromol/L). GABA activated a concentration-dependent inward current, which manifested obvious desensitization. In 58 out of 108 neurons, caffeine induced a small inward current, while in others no detectable current was observed. After the neurons were treated with caffeine (0.1~100 micromol/L) prior to the application of GABA (100 micromol/L) for 30 s, GABA-activated inward currents were obviously inhibited. Caffeine shifted the GABA dose-response curve downward and decreased the maximum response to 57% without changing K(d) value. These results indicate that the inhibitory effect is non-competitive. The pretreatment with caffeine (10 micromol/L) inhibited I(GABA) which was potentiated by diazepam (1 micromol/L). Intracellular application of H-8 almost completely abolished the inhibitory effect of caffeine on I(GABA). Because GABA can induce primary afferent depolarization (PAD), our results suggest that caffeine may be able to antagonize the effect of presynaptic inhibition of GABA in primary afferent.

Effects of L-nitroarginine on the recovery of traumatic facial paralysis / 中华口腔医学杂志

<p><b>OBJECTIVE</b>To study the effects of constitutive nitric oxide synthase inhibitor L-nitroarginine on the recovery of traumatic facial paralysis in rats and the changes of the expression of cNOS and OX42 in the facial nucleus.</p><p><b>METHODS</b>L-nitroarginine was intraperitoneally injected into rats and the recovery of facial paralysis was observed at different time point. and the changes of cNOS and OX42 positive neurons were studied in facial nucleus.</p><p><b>RESULTS</b>Treatment of L-nitroarginine could remarkably inhibit the recovery of traumatic facial paralysis. The cNOS immunoactivity was obvious inhibited in facial nucleus, while the OX42 immunoactivity was obvious increased.</p><p><b>CONCLUSION</b>Endogenous nitric oxide may play an important mediator role on the recovery of traumatic facial paralysis.</p>

Effect of no mediator on kainic acid induced behavioral seizures in rats / 中国应用生理学杂志

<p><b>AIM</b>To further explore the roles of endogenous nitric oxide (NO) or NO derivatives in complex partial seizures and generalized convulsions.</p><p><b>METHODS</b>The effect of pretreatment with L-nitroarginine (L-NNA), an inhibitor of nitric oxide synthase (NOS), or L arginine (L-Arg), a precursor of NO on kainic acid (KA)-induced seizure in rats and the changes in the concentration of NO2 -/NO- in the hippocampus were determined.</p><p><b>RESULTS</b>The rats appeared with wet dog shakes (WDS) at 15 min and then occurred generalized convulsions during 1 h to 3 h after administration of KA (10 mg/kg i.p.). However, the pretreatment of L-NNA (50 mg/kg) so dramatically promoted and enhanced KA-induced behavioral seizures that the latency of generalized convulsion was shorten dramatically, and the mortality was greatly high. In contrast, the pretreatment with L-Arg (40 mg/kg) markedly delayed or weakened KA-induced behavioral changes, such as increasing latency of WDS and generalized convulsion, shortening time o f seizure and none of animal died during observed time. The concentration of NO2- /NO3- in the hippocampus increased immediately at 30 min and remained to 7 d after the administration of KA. Compared with control group (pretreatment with NS), the concentration of NO2- / NO3- in the hippocampus apparently increased at 3 h and 3 d after the administration of KA in the rats with L-Arg pretreatment.</p><p><b>CONCLUSION</b>The endogenous NO (NO or NO derivatives) mediators may play an important role against excitotoxin induced seizures in rats.</p>