ABSTRACT
OBJECTIVE: To describe the CT and MRI features of hepatic sinusoidal obstruction syndrome (HSOS) caused by herbal medicine Gynura segetum. MATERIALS AND METHODS: The CT and MRI features of 16 consecutive Gynura segetum induced HSOS cases (12 men, 4 women) were analyzed. Eight patients had CT; three patients had MRI, and the remaining five patients had both CT and MRI examinations. Based on their clinical presentations and outcomes, the patients were classified into three categories: mild, moderate, and severe. The severity of the disease was also evaluated radiologically based on the abnormal hepatic patchy enhancement in post-contrast CT or MRI images. RESULTS: Ascites, patchy liver enhancement, and main right hepatic vein narrowing or occlusion were present in all 16 cases. Hepatomegaly and gallbladder wall thickening were present in 14 cases (87.5%, 14/16). Periportal high intensity on T2-weighted images was present in 6 cases (75%, 6/8). Normal liver parenchymal enhancement surrounding the main hepatic vein forming a clover-like sign was observed in 4 cases (25%, 4/16). The extent of patchy liver enhancement was statistically associated with clinical severity classification (kappa = 0.565). CONCLUSION: Ascites, patchy liver enhancement, and the main hepatic veins narrowing were the most frequent signs of herbal medicine induced HSOS. The grade of abnormal patchy liver enhancement was associated with the clinical severity.
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Young Adult , Ascites/diagnosis , Asteraceae/chemistry , Cholecystography , Gallbladder/pathology , Hepatic Veins/pathology , Hepatic Veno-Occlusive Disease/chemically induced , Hepatomegaly/diagnosis , Magnetic Resonance Imaging , Phytotherapy/adverse effects , Pyrrolizidine Alkaloids/adverse effects , Severity of Illness Index , Tomography, X-Ray ComputedABSTRACT
This study is to investigate the effect of hydroxyethylpuerarin on the expression of tumor necrosis factor-alpha (TNF-alpha) and activity of nuclear factor kappa B (NF-kappaB) after middle cerebral artery occlusion (MCAO) in rats. Rats were subjected to cerebral ischemia-reperfusion injury induced by MCAO. Hydroxyethylpuerarin (10, 20, 40 mg x kg(-1), iv) was administered just 30 min before occlusion and immediately after reperfusion. After a 24 h reperfusion following 2 h of MCAO, the number of viable neurons in hippocampal CA1 region was counted by hematoxylin and eosin (HE) staining. TNF-alpha protein and its mRNA expression were examined with radioimmunoassay (RIA) and reverse transcriptasepolymerase chain reaction (RT-PCR) respectively. NF-KB activity was observed by electrophoretic mobility shift assay (EMSA), and inhibition of NF-kappaB alpha (IkappaBalpha) protein expression was evaluated by Western blotting analysis. Animals treated with hydroxyethylpuerarin had a significant increase in neuronal survival in comparison with vehicle-treated group. Hydroxyethylpuerarin significantly reduced the protein and mRNA expression of TNF-alpha following 2 h of ischemia with 24 h of reperfusion. NF-kappaB DNA binding activity and the degradation of IkappaBalpha in the cytoplasm also decreased by hydroxyethylpuerarin treatment. The protective effects of hydroxyethylpuerarin against ischemia-reperfusion injury may be mediated by decreasing the expression of TNF-alpha and the activity of NF-kappaB in rats.
Subject(s)
Animals , Male , Rats , Brain , Metabolism , Pathology , Cytoplasm , Metabolism , DNA , Metabolism , I-kappa B Proteins , Metabolism , Infarction, Middle Cerebral Artery , Isoflavones , Pharmacology , NF-KappaB Inhibitor alpha , NF-kappa B , Metabolism , Neuroprotective Agents , Pharmacology , RNA, Messenger , Metabolism , Rats, Wistar , Reperfusion Injury , Metabolism , Pathology , Tumor Necrosis Factor-alpha , GeneticsABSTRACT
The aim of this study is to investigate the effect and mechanism of angiotensin (Ang) II on E-selectin and vascular cell adhesion molecule-1 (VCAM-1) expression in rat brain microvascular endothelial cells (BMEC) and evaluate the effect of compound EXP-2528, a novel Ang II type 1 (AT1) receptor antagonist. The experiment was performed in cultured BMEC of rat. The mRNA and protein expression of E-selectin and VCAM-1 in BMEC was analyzed by RT-PCR and Western blotting, respectively. The results showed that the mRNA and protein expression of E-selectin and VCAM-1 in BMEC were significantly upregulated by 4 h or 18 h exposure to 1 x 10(-7) mol x L(-1) Ang II. These effects were abolished by pretreatment with the selective AT1 receptor antagonists losartan and compound EXP-2528, but not with the AT2 selective antagonist PD123319. Combining losartan with PD123319 also significantly inhibited Ang II-induced E-selectin and VCAM-1 expression in BMEC, but there was no significant difference compared with losartan group. These findings indicated that Ang II upregulated E-selectin and VCAM-1 in BMEC by activating AT1 receptor and then involved in the development of cerebrovascular disease.
Subject(s)
Animals , Rats , Angiotensin II , Pharmacology , Angiotensin II Type 1 Receptor Blockers , Pharmacology , Brain , Cells, Cultured , E-Selectin , Genetics , Metabolism , Endothelial Cells , Metabolism , Imidazoles , Pharmacology , Isoxazoles , Pharmacology , Losartan , Pharmacology , Microvessels , Cell Biology , RNA, Messenger , Metabolism , Vascular Cell Adhesion Molecule-1 , Genetics , MetabolismABSTRACT
<p><b>AIM</b>To evaluate N-acetylaspartate reflecting the neuronal lesion in middle cerebral artery occlusion and reperfusion rat by magnetic resonance spectroscopy (MRS).</p><p><b>METHODS</b>Sixteen adult Wistar rats with MCAO reperfusion and ten pseudooperation rats were performed MRS in vivo at the sixth weeks, then pathologic examination of HE staining and immunohistochemical staining were made. We compared hippocampus modality, cell density and immunohistochemical results with N-acetylaspartate, creatine changes and ration of NAA/Cr.</p><p><b>RESULTS</b>The values of NAA, Cr and NAA/Cr of ipsilateral hippocampus lesion in MCAO reperfusion rats (2.05 +/- 0.33, 2.42 +/- 0.41 and 0.86 +/- 0.10) were visiblly decreased than contralateral hippocampus (3.45 +/- 0.58, 3.10 +/- 0.93, 1.18 +/- 0.32) and control group (3.42 +/- 0.43, 3.57 +/- 0.47, 0.98 +/- 0.14). But the level of decreased NAA is not corresponding to the degree of neuronal death in ipsilateral region of hippocampus in histochemistry.</p><p><b>CONCLUSION</b>MRS has perfect explanation of cell metabolic changes in CA1 region. Decrease of NAA represented neuron delayed injury. But the decreased level of NAA is not perfectly corresponded to the degree of neuron lost. This change has closed correlation with reactive astrocytes proliferation.</p>
Subject(s)
Animals , Female , Male , Rats , Aspartic Acid , Metabolism , Brain Ischemia , Metabolism , Pathology , Hippocampus , Cell Biology , Pathology , Magnetic Resonance Spectroscopy , Methods , Neurons , Metabolism , Pathology , Rats, WistarABSTRACT
0.05).Three days after interventional therapy,the values of BF,BV,MTT,PS,MVD and VEGF of VX_2 tumors in interventional group were (7.5?2.4)ml? 100g~(-1)?min~(-1),(1.20?0.23)ml/100g,(3.29?0.57)s,(4.0?1.5)ml?100g~(-1)?min~(-1), 16.0?2.4/HP and 0.215?0.008 respectively.Compared with the values of pre-interventional therapy and the control group,there were significant differences among them(P0.7,P0.05)but had a significant negative correlation with average A value of VEGF(r=-0.78,P