2.Effect of transfected tissue inhibitor of metalloproteinase-2 on nuclear factor-?B and protein kinase C of the injured rabbit vascular smooth cells
Chinese Journal of Trauma 1993;0(05):-
Objective To study the expression changes of matrix metalloproteinases (MMPs), protein kinase C (PKC) and nuclear factor-?B (NF-?B ) on the injured rabbit vascular smooth muscular cells (VSMC) transfected with tissue inhibitor of metalloproteinase-2 (TIMP-2) vector. Methods Lipofectin method was used to transfect TIMP-2 vector into VSMC, Western blot analysis to detect TIMP-2 peptides and zymography assay to determine MMPs. The activities of MMPs and NF-?B were detected by electrophoretic mobility shift assay (EMSA). The mRNA and protein expressions of PKC? were determined by RT-PCR and immunocytochemistry. Results The injured VSMC showed increased enzyme activity of MMP-2. There was very lower level expressions of PKC? and NF-?B in the normal VSMC but high in the injured VSMC. However, in injured VSMC transfected with TIMP-2 vector, the activity of MMP2/9 was suppressed and the expressions of PKC? and NF-?B decreased (P
3.Great attention should be paid to the adverse drug reactions associated with the use of molecular targeted anticancer drugs.
Zheng-tang CHEN ; Yu-zhong DUAN ; Jian-cheng XU
Chinese Journal of Oncology 2009;31(12):881-884
Antineoplastic Agents
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adverse effects
;
therapeutic use
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Diarrhea
;
chemically induced
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Drug Delivery Systems
;
methods
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Exanthema
;
chemically induced
;
Humans
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Leukopenia
;
chemically induced
;
Lung Diseases, Interstitial
;
chemically induced
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Myocardial Infarction
;
chemically induced
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Neoplasms
;
drug therapy
;
Tumor Lysis Syndrome
;
etiology
4.Electrical stimulation relieves ischemia of rat skeletal muscle via angiogenesis
Lin ZHONG ; Duan CAI ; Bo YU ; Yanling ZHANG ;
Chinese Journal of Physical Medicine and Rehabilitation 2003;0(03):-
Objective To investigate the effects of electrical stimulation on the expression of vascular endothelial growth factor(VEGF)mRNA and receptor FLK 1/KDR in a ischemic model of rat hindlimb. Methods The model of hindlimb ischemia on the right side was established by ligation of the superficial femoral artery in 10 rats. The rats were then randomized into an experimental group and a control group. The rats in the experimental group were intervened with electrical stimulation ( 25 Hz, 0.1 V) on the tibialis anterior (TA) of the right side, while those in the control group were not. RT PCR and immunohistological methods were used to detect the expressions of VEGF mRNA and protein in TA muscles. FLK 1/KDR was detected by means of Western blot and immunofluorescence. Results After 7 days of continuous stimulation, there was a significant increase in blood flow within the muscle. VEGF mRNA and VEGF protein had 4 fold and 2 fold increases, respectively, in the stimulated TA muscles as compared to the control(2.58 vs 0.93, 0.48 vs 0.24, P
5.Three types of induced bursting rhythm in rat injured nerves.
Yu-Bin DUAN ; San-Jue HU ; Zhong JIAN ; Jian-Hong DUAN
Acta Physiologica Sinica 2002;54(4):329-332
Firing patterns of injured nerve fibers were recorded using the single-fiber firing recording technique. Under the same background firing pattern, three types of bursting were induced separately by EGTA, veratridine or high [Ca(2+)](o) in the same type of nerve fibers. The results suggest that different firing patterns are related to different stimuli, which means that each firing pattern carries corresponding neural information.
Action Potentials
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Animals
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Calcium
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pharmacology
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Egtazic Acid
;
pharmacology
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Nerve Fibers
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drug effects
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pathology
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Rats
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Veratridine
;
pharmacology
6.Clinical application of artificial livers.
Chinese Journal of Hepatology 2010;18(11):808-810
Hepatitis
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therapy
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Humans
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Liver Failure
;
therapy
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Liver, Artificial
8.Progress of artificial liver support system technology.
Chinese Journal of Hepatology 2005;13(11):845-846
10.Entecavir treatment causes injury to the mitochondrial DNA of peripheral blood mononuclear cells.
Li ZHOU ; Xiao-yu LIU ; Cai-yan ZHAO ; Zhong-ping DUAN
Chinese Journal of Hepatology 2012;20(10):751-754
OBJECTIVEBased on the potential for nucleotide analogues to affect DNA polymerase-gamma, which controls the proliferation of mitochondria, this study aimed to determine whether long-term treatment with entecavir can cause damage to mitochondrial (mt)DNA in the peripheral blood mononuclear cells (PBMCs) of patients with chronic hepatitis B (CHB).
METHODSPatients with CHB were divided into three groups according to their history of treatment type and duration: (1) entecavir monotherapy for 2 years, n = 17; (2) entecavir monotherapy for 3 years, n = 17; (3) non-antiviral treatment as control, n = 18. PBMCs were isolated and used to assess the mtDNA content by quantitative real-time PCR of mitochondria-specific genes. Plasma malonaldehyde (MDA) and F2-isoprostanes were measured by enzyme linked immunosorbent assay. Plasma total antioxidant capacity (TAOC) was detected by spectrophotometry.
RESULTSThe relative quantity (RQ; of mtDNA to nuclear (n)DNA) was significantly lower in the 3-year treatment group (0.5+/-0.3) than in the control group (1.4+/-1.2; F = 5.233, P = 0.009). The RQ was also significantly lower in the 2-year treatment group (0.4+/-0.2) than in the control group (P = 0.004). The level of F2-isoprostanes (ng/mL) was significantly lower in the 3-year treatment group (1.2+/-0.5) than in the control group (3.6+/-2.9, P = 0.002) or the 2-year treatment group (2.4+/-1.3, P = 0.007). The TAOC was significantly different when compared among all three groups (F = 4.326, P = 0.019). The TAOC (IU/mL) in the 3-year treatment group (2.6+/-1.2) was significantly lower than in the control group (5.0+/-3.0 P = 0.005), but was not significantly different than that for the 2-year group (3.2+/-1.6, P = 0.227). The levels of MDA were not significantly different between any of the groups (F = 0.291, P = 0.749).
CONCLUSIONLong-term treatment with entecavir, up to 3 years, leads to decreased mtDNA content in PBMCs. Since no clinical manifestations of mtDNA toxicity were observed, the consequent damage to the mitochondrial function may be compensated for by yet unknown mechanisms.
Adult ; Antiviral Agents ; adverse effects ; DNA Damage ; drug effects ; DNA, Mitochondrial ; drug effects ; Female ; Guanine ; adverse effects ; analogs & derivatives ; Hepatitis B, Chronic ; blood ; Humans ; Leukocytes, Mononuclear ; cytology ; Male ; Middle Aged