ABSTRACT
Objective To explore the clinical value of ω-3 fatty acids (ω-3PUFA)immune nutrition therapy for the patients with acute ischemic stroke,and analyze its mechanism.Methods 40 patients with acute ischemic stroke were selected.They were divided into the treatment group and the control group,each group in 20 cases. The patients of the control group were given indwelling tube admitted to hospital within 24 hours,given the homogenized meal configured by nutriology department.The treatment group received ω-3PUFA enteral nutrition based on the control group.The neurologic recovery,nutritional status,lipid levels and the incidence of complications were evalua-ted.Results The total effective rate of the treatment group was 90.0%,which was higher than that of the control group (60.0%,χ2 =4.8,P <0.05).The incidence rate of complication of the treatment group was 30.0%,which was lower than the control group (65.0%,χ2 =4.91,P <0.05).The indicators such as NIHSS score,GCS score, TSF and AMC in the treatment group were better than those in the control group[(13.38 ±1.21)points vs.(10.12 ± 1.33)points;(12.9 ±2.6)points vs.(14.1 ±1.7)points;(14.06 ±7.16)mm vs.(14.8 ±4.18)mm;(26.32 ± 1.42)mm vs.(29.40 ±1.08)mm,t =3.51,6.44,3.22,5.19;all P <0.05].TG and LDL -C in the treatment group were lower than those in the control group[(1.60 ±0.71)mmol/L vs.(1.41 ±0.67)mmol/L;(3.11 ±0.60)mmol/L vs.(2.67 ±0.66)mmol/L,t =5.97,4.22;all P <0.05 ].Conclusion The clinical curative effect is better for application of ω-3PUFA on immune nutrition treatment for the patients with acute ischemic stroke.The patients'nerve function,blood lipid levels and nutritional status were significantly improved,and the complications were reduced.
ABSTRACT
Objective To induce experimental allergic encephalomyelitis (EAE) in female C57BL/6 mice with the extracellular domain of myelin oligedendroglia glycoprotein(MOG~(Igd)). Percentages of CD4~+ CD25~+ T cell (Tr) were tested , and also normalized expressions of Foxp3. Methods Molecular cloning technology was used to produce MOG~(Igd) fusion protein. The MOG~(Igd)-TrxA fusion protein and TrxA protein were purified by metal chelate affinity chromatography (MCAC). Mice were injected s. c. in the flank with 300 μg MOG~(Igd) in complete Frcund's adjuvant (CFA) supplemented with 4 μg/μl Mycobacterium tuberculosis. H37Rv. Mice received 0.4 ml emulsion of spinal cord homogenate of guinea pigs (GPSCH) in positive control group, and the same volume emulsiom of TrxA in negative control group, while mice served as normal control received only saline/adjuvant. Mice were monitored two times a day for continuously 30 days by double bind. Clinical scores and histopathology were evaluated. Then, mice were sacrificed. The spinal cord and brain were removed and fixed in buffered formalin. Horizontal sections taken from the central nervous system(CNS) were stained with haematoxylin and eosin (HE), and Kluver-Barrera staining. Also, immunohistochemistry was performed. Percentages of CD4~+ CD25~+ T cells were tested through flow cytometric analysis, and real-time PCR was performed to test normalized expressions of Foxp3 mRNA. Then, correlations between the two were performanced. Results Mice in both MOG group and GPSCH group shew chronic non-remitting course. The onset of disease, time when the most severe clinical symptoms happened and the clinical score between the two groups shew no significant differnces (P>0.05). However, neither in TrxA treated group nor in normal control group did animals exhibit clinical signs of EAE. Histologic sections of the brain and spinal cord taken from affected animals shew perivascular infiltration of mononuclear cells, gliosis, and multifocal demyelination. Lesions scattered throughout the CNS including brainstem, spinal cord, cerebellum, and penventricular white matter. There were significant differences between MOG group and TrxA group in the level of lesion-ceutric AQP-4 expression showing up by immunohistochemistry (P<0.05). Percentages of CD4~+ CD25~+ T cells in MOG group and GPSCH group were (4.71±1.61) % and (1.44±0.65) %, respectively, both of which were significantly lower than those in the normal control group or TrxA treated group (P<0.01). And the difference between MOG group and GPSCH group also reached statistics meaning (P<0.01). Normalized expression of Foxp3 mRNA in MOG group was 2.26± 1.97, and was not significantly higher than the 1.44±1.20 level in GPSCH group (P>0.05). However, they beth were statistically lower than that in the negative control group, namely 8.58±3.34 (P<0.01). Percentages of CD4~+ CD25~+ T cells was statistically correlated with expressions of Foxp3 mRNA (P< 0.05). Conclusion EAE induced in C57BL/6 mice with MOG~(Igd) is reproduceable. It shares the similar clinial signs and pathologic features with human multiple sclerosis(MS). Thus, we find a good way to further study the immune mechanisms of MS and also to search for the effective treatments.