1.Roles of fatty acid transport protein 4 in nonalcoholic fatty liver rats
Aijuan FENG ; Jun WANG ; Dongfeng CHEN
Journal of Third Military Medical University 2003;0(19):-
Objective To study the roles of fatty acid transport protein 4 (FATP4) in rat model of nonalcoholic fatty liver. Methods The fatty liver rat model of high fatty diet (H) was established with a control group (C). The expression of FATP4 genes in fatty liver rats was examined by semi-quantitative reverse transcription and polymerase chain reaction (RT-PCR) and Western blotting. Results In group H, protein and mRNA expressions of FATP4 increased at 2 week, especially at 12 week after high fatty diet (P
2.Inductive effect of high fat diet on uncoupling protein 2 in rats with nonalcoholic fatty liver
Xiaohong GU ; Yundong ZHANG ; Aijuan FENG
Chinese Journal of Tissue Engineering Research 2006;10(32):-
BACKGROUND: Up to now the pathogenesy of nonalcoholic fatty liver(NAFL) is unclear. Uncoupling protein (UCP) of mitochondrial membrane can make oxidative phosphorylation uncoupling in mitochondrium, and then result in decreasing the efficiency of ATP synthesis by mitochondrium and participate the progression of fatty liver by changing energy metabolism.OBJECTIVE: To observe the expressive rule of UCP-2 in NAFL rat models at different time phases.DESIGN: Randomized control animal trial.SETTING: Department of Gastroenterology, Research Institute of Surgery,Daping Hospital, Third Military Medical University of Chinese PLA.MATERIALS: The experiment was performed at National Key Laboratory,Research Institute of Surgery, Daping Hospital, Third Military Medical University of Chinese PLA from November 2004 to December 2005. A total of 64 clean-grade Wistar adult male rats were selected. After being fed with common feed for 1 week, the rats were randomly assigned into model group and normal control group with 32 rats in each group. In each group there were 4 time points: feeding for 2, 4, 8 and 12 weeks, 8 ones at each time point.METHODS: The rats in model group received high fat diet (88% basic feed, 10% pork fat and 2% cholesterol) for 12 weeks. Those in normal control group received common feed in different cages (6 rats in each cage).MAIN OUTCOME MEASURES: Blood was collected from anesthetic rats of the two groups at corresponding time point. Animals were killed,and then liver was extracted rapidly. ①Change of expression of UCP-2in liver was determined with immunohistochemical method and Western blot technique. ②Activity of triacylglycerol, free fatty acid (FFA) and alanine aminotransferase (ALT) in serum was measured with biochemical method. ③Content of malondialdehyde (MDA) in liver tissues was measured.RESULTS: Totally 64 rats were involved in the result analysis. ①Biochemical indicators in serum: Levels of triacylglycerol, FFA and ALT in serum were significantly higher in the model group than in the normal control group at weeks 4, 8 and 12, especially at weeks 8 and 12 (P < 0.01). ②The expression of UCP-2 enhanced gradually with the exacerbation of fatt yliver in the model group, while it was negative in the normal control group.③Content of MDA in liver tissues: It was significantly higher in the model group than in the normal control group at weeks 4, 8 and 12, especially at weeks 8 and 12 [(4.07±0.15), (4.93±0.14), (5.20±0.20) μmol/g; (3.14±0.20), (3.12±0.18), (3.13±0.16) μmol/g,P < 0.01].CONCLUSION: With the formation and aggravation of nonalcoholic fatty liver, levels of triacylglycerol, FFA and ALT in serum and content of MDA in liver tissues increase, and the expression of UCP-2 also increase. It is indicated that high fat diet can induce expression of hepatocyte UCP-2,decrease of ATP progression in cells and accelerate the formation and development of fatty liver.
3.Relationship of expressions of bcl-2, bax and bak with HDAg in tissues of hepatitis D patients
Xiaohong GU ; Aijuan FENG ; Yundong ZHANG ; Qifen LI ; Yuming WANG ;
Journal of Third Military Medical University 2003;0(18):-
Objective To study the roles of apoptosis genes bcl 2, bax, and bak in the pathogenesis of hepatitis D. Methods Expressions of HDAg, bcl 2, bax, and bak in liver specimens of 77 patients with hepatitis D were studied by immunohistochemical method. Meanwhile, the relationship of HDAg expression with the expressions of bcl 2, bax, and bak was studied by double labelling. Results Bcl 2 was mainly expressed in the cytoplasm of hepatocytes, and bax and bak mainly in the cytoplasm of hepatocytes and partly in the nucleus of hepatocytes, and HDAg mainly in the nucleus of hepatocytes. Lots of HDAg and bax/bak positive cells were distributed in infiltrating lymphocytes at the periportal region especially at the advancing edges of areas of piecemeal necrosis. Apoptosis of many hepatocytes was found to locate near the HDAg positive cells. There was positive correlation between the expression of bax/bak and HDAg expression ( P
4.HRCT-Pathological Base of Interface Imaging Asymmetry Distribution in Peripheral Lung Cancer
Fei MENG ; Jingguo WEI ; Wei WANG ; Yaocheng WANG ; Wei GUO ; Aijuan FENG
Journal of Practical Radiology 2001;0(01):-
50%),3 cases speculate that tubecavity didn′t change obviously between cancer lesion and bronchus.The main appearance of bronchiole near lesion distribution was presented as expressed,displacement,going round.There was not constriction obviously or blockage in tubecavity.The main appearance of histology near lesion border was presented as degenerated fibrous tissue envelope and collapse alveoli tissue by lesion expressed.Conclusion The pathological base of interface imaging asymmetry distribution in PLC is bronchial tube emphraxis,lymphatic vessel refluent obstruction,pulmonary interstitial fibrous tissue proliferation,carcinoma infiltration in cancer nodules and lung interface that cancer lesion resulted.
5.Advances in researches on thorax mechanical modeling and simulation during cardiopulmonary resuscitation.
Xinwu XIE ; Qiuming SUN ; Aijuan NI ; Feng TIAN
Journal of Biomedical Engineering 2009;26(3):681-684
Cardiopulmonary resuscitation (CPR) is vital for cardio arrest victims; in this field, researches have been aiming at its mechanism, operation guidelines, new CPR machines and so on. This paper summarized the studies on the mechanical characteristics of the thorax under CPR, and on the simulation work of sternal-displacement relationship in CPR manikins. The data from modeling work showed that the thorax's sternal-displacement relationship could be graphically represented by a hysteresis curve. As the actual CPR manikins' mechanical structures of the thorax are too simplified, it is necessary to do the work of improvement.
Cardiopulmonary Resuscitation
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Computer Simulation
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Heart Arrest
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etiology
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therapy
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Heart Massage
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Humans
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Manikins
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Physical Stimulation
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methods
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Stress, Mechanical
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Teaching Materials
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Thorax
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physiology
6.Pregnenolone 16α-carbonitrile negatively regulates hippocampal cytochrome P450 enzymes and ameliorates phenytoin-induced hippocampal neurotoxicity
Shuai ZHANG ; Tingting WANG ; Ye FENG ; Fei LI ; Aijuan QU ; Xiuchen GUAN ; Hui WANG ; Dan XU
Journal of Pharmaceutical Analysis 2023;13(12):1510-1525
The central nervous system is susceptible to the modulation of various neurophysiological processes by the cytochrome P450 enzyme(CYP),which plays a crucial role in the metabolism of neurosteroids.The antiepileptic drug phenytoin(PHT)has been observed to induce neuronal side effects in patients,which could be attributed to its induction of CYP expression and testosterone(TES)metabolism in the hip-pocampus.While pregnane X receptor(PXR)is widely known for its regulatory function of CYPs in the liver,we have discovered that the treatment of mice with pregnenolone 16α-carbonitrile(PCN),a PXR agonist,has differential effects on CYP expression in the liver and hippocampus.Specifically,the PCN treatment resulted in the induction of cytochrome P450,family 3,subfamily a,polypeptide 11(CYP3A11),and CYP2B10 expression in the liver,while suppressing their expression in the hippocampus.Func-tionally,the PCN treatment protected mice from PHT-induced hippocampal nerve injury,which was accompanied by the inhibition of TES metabolism in the hippocampus.Mechanistically,we found that the inhibition of hippocampal CYP expression and attenuation of PHT-induced neurotoxicity by PCN were glucocorticoid receptor dependent,rather than PXR independent,as demonstrated by genetic and pharmacological models.In conclusion,our study provides evidence that PCN can negatively regulate hippocampal CYP expression and attenuate PHT-induced hippocampal neurotoxicity independently of PXR.Our findings suggest that glucocorticoids may be a potential therapeutic strategy for managing the neuronal side effects of PHT.