BACKGROUND:Cerebral ischemia often occurs in underlying pathological conditions, such as hypertension,
hyperlipidemia and diabetes. Therefore, it is of great significance to construct a cerebral ischemia rat model with hyperlipidemia and to study the effect of basic pathological changes on the cerebral ischemia.
OBJECTIVE:To observe the brain tissue pathological changes of rat models with coexistence of hyperlipidemia and cerebral ischemia, and the effect of hyperlipidmia on cerebral ischemia.
METHODS:The rats were fed with high-fat diet to establish the hyperlipidmia models, and then focal cerebral
ischemia models were prepared with suture method. At 3 and 7 days after modeling, the 2,3,5-triphenyltetrazolium chloride staining was used to observe the volume of brain tissue ischemia, and hematoxylin-eosin staining was
performed to observe pathological change of the margin of the brain tissue ischemia zone.
RESULTS AND CONCLUSION:2,3,5-Triphenyltetrazolium chloride staining staining results showed that the volume of cerebral ischemia was significantly reduced in the hyperlipidemia+cerebral ischemia 7 day group. Hematoxylin-eosin staining results showed there was typical ischemic changes in al the cerebral ischemia models, and the number of microglial cel s after cerebral ischemia for 7 days was significantly smal er than that after cerebral ischemia for 3 days, and the changes were more obvious in the hyperlipidemia+7-day cerebral ischemia group when compared with the hyperlipidemia+3-day cerebral ischemia group. Ultrastructure showed there were neuronal and glial nuclear membrane shrinkage in al the cerebral ischemia models, mitochondria cristae was disappeared completely, endothelial cel mitochondria was decreased, most of the synaptic vesicles of nerve synapse were dissolved;the damages above were improved after ischemia for 7 days, especial y
hyperlipidemia+cerebral ischemia for 7 days, the neuronal degeneration and necrosis were reduced, the
mitochondrial damage was repaired, the number of mitochondrial cristae was increased significantly, and the synaptic vesicles of nerve synapse were recovered significantly. The results indicate that hyperlipidemia can promote the recovery of cerebral ischemic injury,
probably because the hyperlipidemia factors can activate the protection mechanism.

Objective : To study the relationship between lncRNA SIL and proliferation and migration of alveolar epithelial cell during pulmonary fibrosis. Methods : The expression level of lncRNA SIL in A549 cells induced by transforming growth factor(TGF⁃ β1) was detected by RNA fish. The eukaryotic expression vector of lncRNA SIL was built and transfected into A549 cells , the proliferation and migration of the cells after overexpressing lncRNA SIL were studied by RT⁃PCR , MTT , Western blot , cell damage repair experiments and immunofluorescence. Result: The migration and proliferation of A549 cells were significantly reduced compared with the control group after transfected by lncRNA SIL. When lncRNA SIL was overexpressed in A549 cells , cell proliferation , migration and expression of proliferation - related proteins PCNA and Ki67 were decreased compared with the control group. Analysis of the expression of cellular marker proteins showed that , the expression levels of interstitial cell marker proteins α ⁃SMA and Collagen⁃1 were significantly reduced , while the expression level of alveolar epithelial marker protein E. cad significantly increased. Conclusion LncRNA SIL can inhibit the proliferation and migration of A549 cells , and also can inhibit EMT induced by TGF⁃ β1 .

Objective To investigate the role of lncSIL in transforming growth factor-β1(TGF-β1)-induced alveo-lar epithelial interstitial transformation(EMT)and its related signaling pathways.Methods Western blot was used to detect the effect of lncSIL silencing on the expression of E-cadherin(E-cad),alpha-smooth muscle actin(α-SMA)and Collagen I(Col I)in the process of EMT induced by TGF-β1.LncSIL interacting proteins were ana-lyzed by RNA pulldown.Western blot was used to detect the effect of overexpression or silencing of lncSIL on the expression of its target gene enhancer of zeste homolog 2(EZH2)and its downstream factors P21 and cyclin-de-pendent kinase 6(CDK6).Flow cytometry was used to analyze the effect of lncSIL on cell cycle progression.Re-sults After lncSIL silencing,the expression of α-SMA and Col I increased,the expression of E-cad decreased.RNA pulldown assay showed that EZH2 was the target protein that interacted with lncSIL,and the expression of EZH2 increased after silencing lncSIL,the expression of EZH2 downstream gene P21 decreased,CDK6 increased.Flow cytometry showed that the number of cells in S phase significantly increased.When lncSIL was overexpressed,the expression of EZH2 and CDK6 was down-regulated,the expression of P21 was up-regulated,and the number of S phase cells significantly decreased.Conclusion LncSIL inhibits TGF-β1-induced alveolar epithelial cell mesen-chymal transition by negatively regulating EZH2/P21/CDK6 signaling pathway to inhibit cell cycle progression.

【Objective】 To explore the effect of Genistein on the proliferation and cell cycle regulation of ovarian cancer cells. 【Methods】 Ovarian cancer OVCAR-5 cells were treated with Genistein. Cell counting and MTS assays were performed to determine the alterations of cell proliferation. Real-time PCR and Western blotting were conducted to examine the expression changes of key cell cycle regulators. 【Results】 Genistein significantly promoted the proliferation and viability of OVCAR-5 cells. After Genistein treatment, cellular mRNA and protein expression levels of cell cycle activators such as PCNA, Cyclin D1 and CDK4 were increased, but those of cell cycle inhibitors such as p21 and p27 were decreased. 【Conclusion】 Genistein can upregulate the proliferation and G1-S transition of ovarian cancer OVCAR-5 cells. The discrepancy may be caused by diverged experimental conditions and/or different ER expression patterns of cell lines. The findings may provide basic information for in-depth analysis of the role(s) and mechanisms by which genistein confers its effect on ovarian cancer cells.

Poria is an important medicine for inducing diuresis to drain dampness from the middle energizer. However, the specific effective components and the potential mechanism of Poria remain largely unknown. To identify the effective components and the mechanism of Poria water extract (PWE) to treat dampness stagnancy due to spleen deficiency syndrome (DSSD), a rat model of DSSD was established through weight-loaded forced swimming, intragastric ice-water stimulation, humid living environment, and alternate-day fasting for 21 days. After 14 days of treatment with PWE, the results indicated that PWE increased fecal moisture percentage, urine output, D-xylose level and weight; amylase, albumin, and total protein levels; and the swimming time of rats with DSSD to different extents. Eleven highly related components were screened out using the spectrum-effect relationship and LC-MS. Mechanistic studies revealed that PWE significantly increased the expression of serum motilin (MTL), gastrin (GAS), ADCY5/6, p-PKAα/β/γ cat, and phosphorylated cAMP-response element binding protein in the stomach, and AQP3 expression in the colon. Moreover, it decreased the levels of serum ADH, the expression of AQP3 and AQP4 in the stomach, AQP1 and AQP3 in the duodenum, and AQP4 in the colon. PWE induced diuresis to drain dampness in rats with DSSD. Eleven main effective components were identified in PWE. They exerted therapeutic effect by regulating the AC-cAMP-AQP signaling pathway in the stomach, MTL and GAS levels in the serum, AQP1 and AQP3 expression in the duodenum, and AQP3 and AQP4 expression in the colon.
Animals ; Rats ; Poria ; Spleen ; Albumins ; Chromatography, Liquid ; Cyclic AMP Response Element-Binding Protein