Nasal and frontal sinus mucosa of the adult dog contain numerous olfactory sensory neurons and ensheathing glia

Olfactory glial cells have been the focus of much recent research interest because of their possible future use as cellular transplants in repair of spinal cord injury. Although olfactory glial cells can be collected from the olfactory bulb for in vitro culture, alternative sites would be preferable for safer surgical access. This study was designed to investigate the distribution of olfactory sensory neurons and olfactory glial cells within the canine peripheral olfactory system. Using immunohistochemistry and electron microscopy on perfused tissue we demonstrate that olfactory sensory neurons are found in both the caudal nasal and the frontal sinus epithelia. Olfactory ensheathing glia were found in the mucosa at both these sites implying that surgical access for harvesting cells for transplantation would be straightforward.     

Effects of safflor injection on expression of cyclooxygenase-2 mRNA during lung ischemia/reperfusion injury in rabbits

AIM: To investigate the effects of safflor injection (SI) on expression of cyclooxygenase-2 mRNA during lung ischemia/reperfusion injury (PIRI) in rabbits. METHODS: Rabbit lung model of ischemia/reperfusion injury was constructed in vivo. The rabbits were randomly divided into three groups: sham-operation group (group S), ischemia-reperfusion group (group I/R) and ischemia/reperfusion plus safflor injection group (group SI). The lung tissue sampled at the end of the experiment was assayed for wet/dry weight ratio (W/D), injured alveoli rate (IAR) and observed ultrastructure changes under electron microscope. The expressions of COX-1 and COX-2 were measured by immunohistochemistry (IHC). The expression of COX-1 mRNA and COX-2 mRNA were observed by in situ hybridization (ISH). RESULTS: The value of W/D and IAR was much higher in I/R group, but decreased in SI group. Electron microscope showed obvious ultrastructure injury brought by PIRI in I/R group, which was greatly attenuated in SI group. The IHC and ISH demonstrated that COX-2 and COX-2 expressions in pulmonary tissue of I/R group were significantly higher than those in S group (P<0.01). The difference of COX-1 and COX-1 expressions in pulmonary tissue was not observed among three groups. CONCLUSION: The lung ischemia-reperfusion insult induces the up-regulation of COX-2 in lung. Safflor injection may attenuate lung ischemia-reperfusion injury through inhibiting COX-2 expression.     

Role of vascular remodeling for urotensin Ⅱ in rat thoracic aorta after balloon injury

AIM: To explore the possible effect of UII in the process of remodeling after vascular injury. METHODS: The rat model of balloon injury in thoracic aorta was established. Male rats were randomized to 4 groups (n=5), including sham injury group, injury group, UII group (UII pumped into the rats after thoracic aorta balloon injury at 1.0 nmol·kg-1·h-1) and urantide group (urantide pumped into the rats after thoracic aorta balloon injury at 10 nmol·kg-1·h-1). At 21 days, the thoracic aortas were taken out to measure the changes of pathology, the expression of UII, the proliferation of VSMC and the expression of collagen. RESULTS: (1) At the 21 days after operations, the systolic blood pressure was higher in UII group than that in injury group ［(140.0±10.0) mmHg vs (132.0±3.4) mmHg, P>0.05］. The systolic blood pressure was also obviously higher than that in urantide group ［(140±10.0) mmHg vs (128.0±2.4) mmHg, P<0.05］. (2) Urotensin Ⅱ was expressed strongly in the injured area after thoracic aorta injury. (3) In contrast to injury group, the intimal thicken in urotensin Ⅱ group enhanced, the decrease in lumen area was marked (0.13±0.05 vs 0.07±0.02, P<0.05), the cell proliferation index was markedly increased (0.74±0.16 vs 0.40±0.11, P<0.01), and the expression of collagen was also markedly increased (counted as IOD, 318±127 vs 78±26, P<0.01). (4) In contrast to injury group, the decrease in lumen area was not abolished (0.09±0.03 vs 0.07±0.02, P>0.05) after chronic infusion of urotensin Ⅱ receptor antagonist urantide, the cell proliferation index was markedly increased (0.73±0.15 vs 0.40±0.11, P<0.01) and the expression of collagen was not statistically increased (counted as IOD, 200±79 vs 78±26, P>0.05). CONCLUSION: Urotensin Ⅱ expresses strongly in the myointimal cells after thoracic aorta injury in rat. The extra UII enhances the proliferation of VSMC and expression of collagen in the myointimal, increases the stenosis of injured vasculature, indicating that UII might take part in the process of repairing after vessel injury.     

Effect of preconditioning with pioglitazone on ischemia reperfusion/hypoxia reoxygenation-induced mitochondrial structure and membrane potential in rats

AIM: To observe the effect of preconditioning with pioglitazone on ischemia reperfusion/hypoxia reoxygenation-induced mitochondrial ultramicro-structure and membrane potential in rats. METHODS: Sprague-Dawley rats were randomly divided into four groups: sham-operated (SO) group, ischemia reperfusion (IR) group, pioglitazone preconditioning group (Pio-P) and 5-HD+pioglitazone (5-HD+Pio) group. Apart from the SO group, IR, Pio-P and 5-HD+Pio groups were subjected to 30 min ischemia and 4 h reperfusion. The heart was quickly removed for observing the structure of mitochondria and measurement of the apoptosis index (AI) by TUNEL. Primary cultured cardiomyocytes of Sprague-Dawley rats were divided into control, hypoxic reoxygenation (HR) and different concentrations of Pio-P group. JC-1 staining flowcytometry was adopted to examine mitochondrial membrane potential (ΔΨm). RESULTS: The injury of mitochondrial structure in IR group was severer than that in Pio-P group, while the difference between 5-HD+Pio group and IR group was not evident. Flameng score in Pio-P group(1.62±0.60) was significantly lower than that in IR group (2.75±1.09), P<0.01. AI in Pio-P group (28.19%±4.93%) was lower than that in IR group (55.44%±6.63%),P<0.05. The rates of low ΔΨm cells in (5 μmol/L,10 μmol/L and 15 μmol/L) Pio-P group were (45.89±3.63)%, (17.13±1.37)% and (18.43±2.44)%, significantly lower than that in HR group (56.52%±2.87%),P<0.05, while the difference between 10 μmol/L group and 15 μmol/L group was not significant (P>0.05). CONCLUSION: Pioglitazone protects the heart from ischemia reperfusion/ hypoxia reoxygenation injury evidenced by improving mitochondrial ultrastructure and lessening the loss of mitochondrial membrane potential, and decreasing apoptosis. The cardioprotective effects can be inhibited by the blocker of mitochondrial ATP-sensitive potassium channels.     

Hepatoprotective effect of Paecilomyces tenuipes polysaccharides on carbon tetrachloride -induced liver injury

AIM:To investigate the protective effect of crude Paecilomyces tenuipes polysaccharides (cPtPs) and Paecilomyces tenuipes polysaccharides (PtPs) in a rat model of acute hepatic necrosis induced by carbon tetrachloride (CCl4). METHODS:Wistar rats were divided into four groups (control group, CCl4 group, cPtPs+CCl4 group and PtPs +CCl4 group), the four groups were given intragastrically with normal saline, cPtPs and PtPs for 15 d, respectively. In the last two days, these groups except control group were injected peritoneally with CCl4. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL), direct bilirubin (DBIL) and indirect bilirubin (IBIL) were detected by automatic biochemistry analyzer. Pathological changes of hepatic tissue were assessed by hematoxylin-eosine (HE) staining. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in liver homogenate were analyzed using xanthinoxidase and thio-barbituric acid, respectively. The concentration of Ca2+ in hepatocyte mitochondria was determined by colorimetric method. The expression of α-smooth muscle actin (α-SMA) was examined in hepatic tissue by immunohistochemical method. RESULTS:Compared with control group, serum levels of ALT, AST, TBIL, DBIL and IBIL in CCl4 group increased significantly, denaturation and necrosis implicated to the whole hepatic lobules. Compared with CCl4 group, serum levels of ALT, AST, TBIL, DBIL and IBIL in PtPs +CCl4 group decreased significantly, denaturation and necrosis located in the third region of hepatic lobules, the level of SOD increased and MDA decreased (P<0.05) in endochylema. Concentration of Ca2+ in mitochondria decreased in PtPs +CCl4 group and cPtPs +CCl4 group (P<0.05, P<0.01, respectively). Expression of α-SMA was found little in PtPs+CCl4 group. CONCLUSION:PtPs, the effect is better than cPtPs, lessens CCl4-induced hepatonecrosis significantly. The role may be related with anti-lipid peroxidation.     

1-MCP对不同成熟度白凤桃冷害发生的影响

以白凤桃果实为材料,研究了1-甲基环丙烯(1-MCP)对低温冷藏条件下果实成熟生理和冷害发生的影响。实验采用25μL/L1-MCP分别对底色转白期(MG)和成熟期(RR)桃果实进行处理,然后置于(0±1)℃冷库中贮藏24d。结果表明,1-MCP处理都能够延缓MG和RR果实的后熟软化进程,降低乙烯释放量,并抑制了果实快速软化阶段的PG酶活性;1-MCP处理提高了贮藏后期MG果实的硬度,降低了出汁率,加剧了冷害的发生程度,1-MCP处理对RR果实的冷害发生率没有显著影响,表明1-MCP对桃冷害的发生程度与果实成熟度有关。     

Time-course changes in the expression levels of miR-122, -155, and -21 as markers of liver cell damage,inflammation, and regeneration in acetaminophen-induced liver injury in rats

Drug-induced liver injury (DILI) is a significant threat to patient health and a major concern during drug development. Recently, multiple circulating microRNAs (miRNAs) have been reported to be potential biomarkers for DILI. To adapt and validate miRNAs for clinical use, we investigated the time-course changes in miR-122 expression levels in an acetaminophen-induced liver injury model in rats. In addition, miR-155 and miR-21 were evaluated as makers of inflammation and regeneration, respectively, to characterize liver status. Our results revealed that miR-122 is an early and sensitive biomarker of hepatocellular injury at a stage when alanine transaminase, aspartate transaminase, and total bilirubin were not detectable. However, no significant differences in the expression levels of other miRNAs (miR-155 and -21) were observed between treatment and vehicle groups. Collectively, these time-course changes in the expression levels of miRNAs may be useful as markers for clinical decision-making, in the diagnosis and treatment of DILI.     

Variation of CD8 after traumatic brain injury in serum of rats

AIM: To explore the character of CD8 after traumatic brain injury (TBI) in peripheral blood. METHODS: Improved Feeney's free-fall method was used to set up traumatic brain injury model. The levels of neuron-specific enolase (NSE) and CD8 in the serum of the rats were detected by ELISA. The correlation of both NSE and CD8 in the serum was analyzed by Pearson product-moment correlation. The FasL expression in the lymphocytes of peripheral blood was determined by Western blot. RESULTS: The elevated level of CD8 lagged behind the level of NSE in the serum after TBI. The serum level of NSE was significantly increased at the 1st day after TBI and reached a peak at the 3rd day, subsequently gradually decreased to a lower level; the serum level of CD8 was increased at the 3rd day after TBI, and reached a peak at the 7th day, then gradually decreased. The serum levels of NSE at 1st, 3rd and 7th days were positively correlated with the serum level of CD8 at 3rd, 7th and 14th days. However, the FasL expression in the CD8⁺ lymphocytes of peripheral blood showed no variation at different time points after TBI. CONCLUSION: NSE in the serum released from neural tissues after TBI stimulates immune response and induces the augmentation of CD8 in peripheral blood, which may be a cause of secondary injuries in the brain.