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Objective:To investigate the relationship between intracranial arterial remodeling and imaging markers in patients with cerebral small vessel disease (CSVD).Methods:One hundred and fifty-six patients with CSVD who were admitted to the Department of Neurology of the Second Affiliated Hospital of Zhengzhou University or the Public People′s Hospital of Xinzheng from January 2020 to May 2022 were selected, and their brain artery remodeling (BAR) score was calculated. The patients with BAR score≤-1 standard deviation (SD) were defined as individuals with constrictive remodeling of intracranial arteries, and the patients with BAR score≥1 SD were defined as individuals with dilated remodeling of intracranial arteries. Imaging markers of CSVD [white matter hyperintensities (WMHs), lacune, cerebral microbleeds, enlarged perivascular spaces, and cerebral atrophy] were quantified, total CSVD load was calculated and patients were divided into low load group (0-2 points, n=91) and high load group (3-4 points, n=65) according to the total CSVD load scores. The correlation between intracranial artery remodeling and various imaging markers of CSVD and total load was analyzed by using univariate analysis and binary Logistic regression analysis. A nomogram prediction model was established and a receiver operating characteristic curve (ROC) was drawn to assess the predictive value of intracranial artery remodeling on high total CSVD load. Results:Dilated intracranial arterial remodeling was an independent influence factor on severe WMHs ( OR=3.66, 95% CI 1.38-9.72, P=0.009), lacune ( OR=3.78, 95% CI 1.17-12.19, P=0.026), cerebral atrophy ( OR=3.11, 95% CI=1.10-8.81, P=0.033), and high total CSVD load ( OR=6.66, 95% CI=2.14-20.77, P=0.001). Age was an independent influencing factor for high total CSVD load ( OR=1.12, 95% CI 1.07-1.16, P<0.01). A nomogram prediction model for high total CSVD load with age and BAR score≥1 SD as dependent variables had a good effect (C-index=0.826) and calibration ( P=0.024). The best cut-off point of ROC curve was 0.50, with an area under the curve of 0.83 (95% CI 0.76-0.89, P<0.01), the sensitivity and specificity of 0.72 and 0.82. Conclusions:Patients with dilated intracranial arterial remodeling may have a heavier CSVD load. Dilated intracranial arterial remodeling may serve as a new biomarker for assessing CSVD, but the mechanism of the association needs further study.
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Objective:To investigate the clinical and imaging features of bilateral Wallerian degeneration of the middle cerebellar peduncles secondary to isolated pontine infarction.Methods:Patients diagnosed as bilateral Wallerian degeneration of cerebellar middle peduncle after isolated pontine infarction admitted to the Second Affiliated Hospital of Zhengzhou University from June 2017 to December 2021 were retrospectively included. Patients with bilateral Wallerian degeneration of cerebellar middle peduncle after isolated pontine infarction reported between January 2001 and December 2021 were collected by searching Chinese and English databases, and their clinical and imaging characteristics were summarized.Results:A total of 48 patients with bilateral Wallerian degeneration of cerebellar middle peduncle after isolated pontine infarction were included, including 14 patients admitted to the Second Affiliated Hospital of Zhengzhou University, and 34 patients collected by searching the Chinese and English databases. Thirty-three patients were males (68.75%) and 15 were females (31.25%). Their age was 65.8±10.7 years old (range, 37-88 years). Most patients had vascular risk factors, and hypertension was the most common. Dysarthria and limb weakness were the main clinical symptoms at admission. The infarct sites of all 48 patients were located in the blood supply area of paramedian pontine arteries, of which 37 (77.08%) were unilateral (18 on the left and 19 on the right), 6 (12.50%) were bilateral sides, and 5 (10.42%) had incomplete data. When Wallerian degeneration was diagnosed, 8 patients (16.67%) had dizziness or ataxia, 6 (12.50%) had aggravated original symptoms, and the remaining 34 (70.83%) had no new symptoms or aggravated original symptoms. All patients showed symmetrical abnormal signals in bilateral middle cerebellar peduncles, with obvious hyperintensity on T 2 or diffusion-weighted imaging (DWI). One patient showed T 2 hyperintensity in bilateral middle cerebellar peduncle on the next day after the onset of the infarction, which was the earliest case to find secondary Wallerian degeneration after isolated pontine infarction. Conclusions:Wallerian degeneration should be considered when symmetrical lesions of bilateral middle cerebellar peduncles occur after isolated pontine infarction. Wallerian degeneration may occur early after isolated pontine infarction. Most cases have no new symptoms or aggravated original symptoms. Conventional MRI can identify it early.
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Objective To explore the potential mechanism of action of estradiol benzoate on proliferation and differentiation of rat hippocampal neural stem cells.Methods Hippocampus tissues from SD rats were dissociated and plated into culture flasks.Neural stem cells were identified by immunofluorescence against Nestin.After treatment with different concentration of estradiol benzoate (10-10,10-9,10-8,10-7,10-6 mol/L),the proliferation and differentiation of neural stem cells were assessed by MTT assay and the proportion of neurons and astrocytes in differentiated cells was assessed by flow cytometry.Western blot assay was performed to detect the expression levels of protein in neural stem cells.Results (1) The neural stem cells formed neurospheres and grew in floating,and were Nestin-positive.Estrogen receptors,including ERα and ERβ,were expressed in neural stem cells;(2)After treatment with 10-8 mol/L estradiol benzoate versus in the control group,the cell viability was significantly increased (t =5.36,P =0.003),and the ratio of neuron-specific nuclear protein(NeuN)-positive neuron cells in total cells was significantly increased (t =4.32,P =0.02),but the ratio of glial fibers acidic protein(GFAP)-positive cell in total cells was decreased(t=4.65,P=0.008).The expression levels of GDNF,GFRal and Ret proteins were enhanced in the estradiol benzoate group compared with the control group.Conclusions Appropriate concentration of estradiol benzoate promotes proliferation and differentiation ofin vitrocultured hippocampal neural stem cells and elevates the ratio between neurons and glial cells differentiated from neural stem cells.
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Objective To study adipose-derived stem cells (ADSCs)differentiation into endothelial cells and smooth muscle cells by induction with supernatant liquid from cerebral infarction tissue in rats.Methods The ADSCs were obtained from retroperitoneal adipose tissue of rats and identified by flow cytometry technology.The normal brain tissues and the infarcted cerebral tissue obtained from rats with middle cerebral artery occlusion were used to induce ADSCs differentiation,and no intervention group was as a control.The mRNA expression level of von willebrand factor (vWF),α-smooth muscle actin (α-SMA) and smooth muscle myosin heavy chain (SM-MHC) in cells after induction were detected using reverse transcriptase-polymerase chain reaction.Immunofluorescence were used to identify the expression of endothelial cells markers and smooth muscle cell markers,and positive expression cell was detected by fluorescence microscope.Results On the ADSCs surfaces,the high expressed-positive antigens included CD90 (96.7％),CD29 (84.4％),CD44 (98.9％),and the low expressed negative antigens included CD45 (6.5％),CD34 (7.4％) and CD31 (3.6％).Compared with no intervention group and normal brain tissue of supernatant liquid group,the cerebral infarction tissue of supernatant liquid-induced group showed the increased mRNA expression level of vWF,α-SMA and SM-MHC(F=5.962,6.756,6.144,P=0.001,0.004,0.003),and showed that the immunofluorescence indicated-cell expression level of vWF,α-SMA and SM-MHC was much more increased (all P ＜ 0.05).Conclusions Under the induction by supernatant liquid of cerebral infarction tissue,ADSCs highly expresses the markers of endothelial cells and smooth muscle cells.This suggests that the cerebral infarction tissue of supernatant liquid-induced ADSCs have a tendency to differentiate into endothelial cells and smooth muscle cells.
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Objective To observe the effect of the three active ingredients of a Chinese traditional medicine compound named Kang Fu Ling( KFL) against PC12 cells oxidative damage induced by microwave radiation.Methods PC12 cells were differentiated into neuros induced by nerve growth factor ( NGF ) .PC12 cells were incubated for 48 hours after astragalosides,total paeony glycoside and tanshinones were added at different concentrations (1, 3, or 9 μg/ml) .The cells in the control group were cultivated with the only medium of the same volume.Then, cells were irradiated with 30 mW/cm2 microwave for 6 minutes.The morphology of PC12 cells was observed under an inverted microscope soon before and after irradiation and the cell viability was measured by methylthiazolyl tetrazolium ( MTT) colorimetry.Reactive oxygen species ( ROS ) was determined using active oxygen probe 2′, 7′-dichlorodihyarofluolescen diacetde ( DCFH-DA ) while malonyldialdehyde(MDA) was measured in the homogenate of PC12 cells through thiobarbituric acid ( TBA) reactive substance assay.Results The cell morphology of each group showed no obvious difference.6 h after irradiation, the viability of irradiation control group measured by MTT declined apparently(P<0.01)compared with the normal control group.The 3 μg/ml astragalosides treatment group increased the viability of PC12 cells after microwave exposure ( P <0.01).The contents of ROS and MDA were increased after irradiation(P<0.01).However, in the three active ingredients of Kang Fu Ling treatment groups, both ROS and MDA were much lower than in irradiation control group.Conclusion Astragalosides, total paeony glycoside and tanshinones, which are the three active ingredients of Kang Fu Ling, all have protective effect against PC12 cell injury caused by microwave radiation,possibly by scavenging free radicals and reducing oxidative stress injury.
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BACKGROUND: Basic fibroblast growth factor (bFGF) possesses multiple functions such as promoting neuronal survival and growth of cell processes in vitro and antagonizing the toxicity of excitatory amino acids,thereby playing import roles in functional recovery of the central nervous system (CNS). But whether bFGF offers neuroprotection on ischemic brain tissues by modulating intracellular free calcium content remains unknown.OBJECTIVE: To explore the effect of bFGF on intracellular free Ca2+ in the neural cells in the event of focal cerebral ischemia-reperfusion (IR)injury.DESIGN: Randomized controlled study.SETTING: Department of Neurology of Second Hospital Affiliated to Zhengzhou University.MATERIALS: This study was conducted in the Laboratory of the Department of Neurology, Second Hospital Affiliated to Zhengzhou University between August and December 2003. Totally 24 SD were randomized into sham operation group, ischemic group, IR group and bFGF exposure group with 8 rats in each group.METHODS: Middle cerebral artery occlusion (MCAO) model was established in rats in IR group and bFGF exposure group by inducing arterial thrombosis with thread, which was not preformed in rats in the sham operation group. Rats in bFGF exposure group received intraperitoneal injection of 10 μg/kg bFGF immediately after ischemia,which was replaced by the same volume of physical saline in the other two groups. Free Ca2+ in brain cells was detected at 24 hours of IR.MAIN OUTCOME MEASURES: Free Ca2+ in the brain cells at 24hours of IR.RESULTS: All the 24 rats survived the experiment. Free Ca2+ in IR group was significantly higher than that of the sham operation group [(673.46±18.44) vs (224.71±10.58) nmol/L, F=1 329.06, P ＜ 0.01], and also significantly higher in bFGF exposure group [(378.37±21.08) nmol/L,F=1 329.06, P ＜ 0.01].CONCLUSION: Intracellular free calcium can be obviously depressed by bFGF following IR injury, which benefits cell membrane stability and help prevent intracellular Ca2+ overload.