1.THE PROTECTIVE EFFECTS OF FOLIC ACID,VB_6,VB_(12) TO RAT AORTIC ENDOTHELIAL CELLS INJURIED BY DL-HOMOCYSTEINE
Acta Nutrimenta Sinica 1956;0(01):-
Objective:To investigate the cross protective effects of folic acid,VB6,VB12 on rat aortic endothelial cells(RAEC) from injury induced by DL-homocysteine(Hcy).Method:RAEC were cultured in vitro,and the cross effects of folic acid,VB6,VB12 were studied by MTT.According to the results of orthogonal design,the activities of SOD,GSH-PX,NOS and the contents of MDA,NO in the media were compared.Results:The results of orthogonal design indicated that the inhibition of Hcy to RAEC could be relieved by folic acid,VB12 excluding VB6.The interaction existed between folic acid and VB12,as well as VB6 and VB12.The inhibition of Hcy to the enzymes(SOD、GSH-PX、NOS) could be relieved by three vitamin projects.Folic acid,VB12,VB6 could inhibit the reduction of NO and decrease the production of MDA.Conclusion:The simultaneous addition of folic acid,VB6 and VB12 may be an excellent strategy for protection of RAEC injury induced by DL-homocysteine.
2.EFFECT OF DL-HOMOCYSTEINE ON EXPRESSION OF VCAM-1 AND ADHESION BETWEEN ENDOTHELIAL CELLS AND MONOCYTES IN VITRO
Acta Nutrimenta Sinica 1956;0(02):-
Objective: To investigate the effect of DL-homocysteine (Hcy) on expression of VCAM-1 and the adhesion between endothelial cells and monocytes in cultured rat aortic endothelial cells. Method: Rat aortic endothelial cells were cultured in vitro and treated by 0-5.0 mmol/L Hcy for 24 h. The activity of SOD and GSH-Px, the contents of MDA in the medium and the rates of adhesion between endothelial cells and monocytes were determined. The expressions of NF-?b,VCAM-1 protein and the VCAM-1 mRNA were detected by immunocytochemical and reverse transcriptase PCR respectively. Results: Compared with control group and 0.01 mmol/L Hcy , 0.1-5.0 mmol/L Hcy significantly inhibited the activity of SOD and GSH-Px, increased the contents of MDA and the expression of NF-?B and VCAM-1mRNA, enhanced the rates of adhesion between endothelial cells and monocytes. Conclusion: Homocysteine may play a crucial role in atherosclerosis by increasing the expression of NF-?B,VCAM-1mRNA and enhancing the rates of adhesion between endothelial cells and monocytes.
3.A SEVEN-MONTH-OLD INFANT WITH NIEMANN PICK DISEASE:A CASE REPORT
Modern Hospital 2015;15(5):59-60
Objective To study the various clinical manifestations of niemann pick disease, and to improve the ability of diagnosis and differential diagnosis in order to reduce misdiagnosis or missed diagnosis.Methods The onset and diagnostic procedure of a seven-month-old infant with niemann pick disease were reported and relative literature were reviewed and studied.Results The infant demonstrated severe hepatosplenomegaly, abnormity of liver function, anemia and development backwardness.Bone marrow examination indicated storage cells suggestive of niemann pick cells.Conclusion Niemann pick disease is a group of rare diseases with various clinical manifestations. Clinical suspected cases need further bone marrow examination, pathologcal biopsy and gene tests.
4.Protective effect of schisandrin B against HK-2 apoptosis induced by Cisplatin
Chinese Pharmacological Bulletin 2014;(7):961-964
Aim To explore the protective role of schisandrin B (SchB)against HK-2 damage induced by Cisplatin and the probable mechanism.Methods Cultivated HK-2 was interacted by Cisplatin and SchB with different concentrations.Invert microscope showed cellular form change and Flow Cyto Meter told apopto-sis.Combined with test result on the change of L-DH, MDA and LPO,probable protective effect of SchB on HK-2 was studied and analyzed.Result Cisplatin in-hibited cells′growth and induced apoptosis.20 μmol · L-1 SchB significantly reduced apoptosis of Cispla-tin-induced HK-2,and offered the best protection. SchB could reduce MDA,LPO,LDH significantly in-creased by cisplatin.Conclusion SchB can be an ef-fective inhibition agent of Cisplatin-induced renal tubu-lar epithelial cell apoptosis (HK-2 ).The mechanism can be the inhibition of Cisplatin-induced oxidative stress by antioxidant effect.
5.A report of four cases of hemolytic disease caused by red blood cell immune in neonates antibodies
Journal of Clinical Pediatrics 2015;(6):562-566
Objective To investigate the laboratory ifndings, clinical manifestations and treatment in hemolytic disease caused by red cell immune antibodies in neonates. Methods The laboratory and clinical data from 4 cases of hemolytic disease of neonates caused by red cell immune antibodies were retrospectively analyzed. Results IgG antibody were detected in all mothers of 4 cases during pregnancy and they were anti-E, anti-D, anti-Jkb and the autoantibody with the titer being 16, 2048, 1 and 16 respectively. The four neonates were all full-term. The jaundice appeared 6 h to 3 d after birth with varying degrees of skin stained yellow, with or without anemia. Serology and elution test found the existence of antibody same as the one on their maternal red cells and the titer was 4, 512, 0, and 2, respectively. All neonates were treated by phototherapy. Two servere cases were also treated by whole blood exchange and red blood cells transfusion. The prognosis were good in all neonates. Conclusions Prenatal immune hematological tests facilitated early detection of irregular erythrocyte antibodies and thus assessment of the risk of hemolytic dis-ease of the fetus and neonates.
6.Association of human ghrelin gene polymorphism with type 2 diabetes mellitus
Basic & Clinical Medicine 2006;0(01):-
Objective To study the relationship between ghrelin gene polymorphisms and type 2 diabetes.MethodsAll subjects were genotyped for these two single nucleotide polymorphisms(C408A,G346A)of ghrelin by PCR-RFLP assay.Anthropometric variables,blood glucose,insulin,lipid,uric acid and other clinic parameters were measured.Results In control group,the genotype frequencies are as follows:CC 75.4%(n=251),CA 24.0%(n=80),and AA 0.6%(n=2).In type 2 diabetes group,the genotype frequencies are as follows:CC 70.8%(n=143),CA 28.2%(n=57),and AA 1.0%(n=2).There was no significant differences of the genotype frequencies in two groups.In control group,serum total cholesterol in subjects carrying CC genotype was higher than that of subjects without CC genotype(P
7.Effect of formaldehyde inhalation on allergic rhinitis in mice.
Journal of Clinical Otorhinolaryngology Head and Neck Surgery 2015;29(16):1467-1471
OBJECTIVE:
To observe the effect of formaldehyde inhalation on the allergic rhinitis mice model.
METHOD:
Forty-eight male BALB/C mice in six experimental group were exposure to (A) saline control; (B) Der p1; (C) formaldehyde (3.0 mg/m3); (D) Derp1 + formaldehyde (1.5 mg/m3); (E) Der p1 + formaldehyde (3.0 mg/M3); (F) Der p1+ formaldehyde (6.0 mg/m3). The concentrations of IL-4, IL-10 and IFN-γ in the peripheral serum were measured by enzyme-linked immunosorbent assay(ELISA). Nasal mucosal inflammation was evaluated by HE staining. Result: Formaldehyde exposure could increase the number of allergic rhinitis mice with sneezing and rubbing nose. The levels of IL-4 and IL-10 in group B, D, E and F were higher than that ingroup A (P < 0.05). Compared with the group C, the group D, E and F could effectively increase serum IL-4 and IL-10. The concentration of IL-4 in group E and F was higher than that of group B, while the group C was lower (P < 0.05). The concentration of IL-10 in group D, E and F was higher than that in group B (P < 0.05). The expression of IFN-γ in group B, D, E and F was lower than that in group A. While, the IFN-γ expression in group B was lower than that of group C and higher than that in group F (P < 0.05). Moreover, the concentration of IFN-γ in group D, E and F was lower compared with group C (P < 0.05). The nasal mucosa HE staining showed that the density of EOS increased simultaneously in formaldehyde exposure allergic rhinitis groups.
CONCLUSION
The study showed that formaldehyde exposure can promote Th2 cytokines and eosinophil infiltration and then aggravate the allergic rhinitis symptoms.
Animals
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Antigens, Dermatophagoides
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Arthropod Proteins
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Cysteine Endopeptidases
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Disease Models, Animal
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Enzyme-Linked Immunosorbent Assay
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Formaldehyde
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adverse effects
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Inflammation
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Inhalation Exposure
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adverse effects
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Interferon-gamma
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blood
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Interleukin-10
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blood
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Interleukin-4
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blood
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Male
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Mice
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Mice, Inbred BALB C
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Nasal Mucosa
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Rhinitis, Allergic
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chemically induced
8.Platelet-rich plasma accelerates the proliferation of bone marrow mesenchymal stem cells
Chinese Journal of Tissue Engineering Research 2015;(14):2144-2148
BACKGROUND:Platelet-rich plasma contains a variety of stimulating factors, and can also raise the proteoglycan and col agen synthesis. OBJECTIVE:To observe the effect of platelet-rich plasma on the proliferation of goat bone marrow mesenchymal stem cel s. METHODS:Blood samples were extracted from the jugular vein of Inner Mongolia Ximeng goats to harvest platelet-rich plasma using centrifugation method. Then, bone marrow was extracted from the goat’s ilium by puncture method to isolate and purify goat bone marrow mesechymal stem cel s using density gradient centrifugation method. After that, primary cel s at good state were cultured in L-DMEM complete medium containing 10%, 20%, 30%platelet-rich plasma or in simple L-DMEM complete medium. RESULTS AND CONCLUSION:Within 2-6 days of culture, cel s in the platelet-rich plasma groups proliferated faster than those in the control group, and with the increasing of platelet-rich plasma concentration, the cel s grew faster, with larger number and more mature morphology. At 4 days of culture, the cel doubling time was about 50, 35, 25 hours in the 10%, 20%, and 30%platelet-rich plasma groups, respectively. These findings indicate that goat platelet-rich plasma can dramatical y promote the proliferation of bone marrow mesenchymal stem cel s in a concentration-dependent manner.
9.Moyamoya disease and immune inflammation
International Journal of Cerebrovascular Diseases 2016;24(2):146-149
Moyamoya disease is a chronic progressive cerebrovascular disease. Its main manifestation is bilateral internal carotid artery progressive stenosis w ith abnormal vascular netw ork formation of the compensatory hyperplasia in brain base. The pathological mechanism of moyamoya disease is not clear. Grow ing evidence has suggested that immune inflammation may play an important role in its occurrence and development process. Abnormal expression of various inflammatory cytokines and immune proteins can be observed in patients w ith moyamoya disease. This article review s the possible mechanism of immune inflammation in moyamoya disease in recent years.
10.High-mobility group protein B1 and ischemic stroke
International Journal of Cerebrovascular Diseases 2016;24(3):263-267
High mobility group protein box 1 (HMGB1) is a typical nonhistone chromosomal protein. It has many celular functions in nucleus. Studies in recent years have showed that HMGB1 can be released to the outside of cels to exert a wide range of cytological effects. Ischemic stroke is one of the diseases with the highest morbidity and disability. More and more evidence has shown that HMGB1 plays a variety of important roles in the occurrence and development process of ischemic stroke. This article reviews the roles of HMGB1 in ischemic stroke.