Objective Disorder of intestinal barrier function is associated with the non-alcohol fatty liver disease ( NAFLD) . The present paper aimed to explore the intestinal barrier function in the rat model of NAFLD . Methods Sixteen SD rats were ran-domly divided into an NAFLD and a normal control group of equal number .The NAFLD models were constructed by high-fat feeding . HE staining was used for pathologic examination of the liver , the levels of TNF-α, IL-1, and endotoxin (ET ) were measured by ELISA and the limulus reagent method , and the expressions of intestinal ZO-1 and Occluding were determined by real time PCR . Resu lts Compared with the normal controls , the NAFLD rats showed typical hepatic lipid deposition , with significantly increased levels of serum TNF-αand IL-1 and plasma ET and decreased expressions of intestinal ZO-1 and Occluding (P<0.05). Conclusion Intestinal barrier function is decreased in NAFLD rats .

Anything in the universe can be explained by Yin-yang theory of Chinese medicine. Synaptic connections in the central nervous system also embody a balance between Yin and Yang. To discover the synaptic processes of gathering,storing and retrieving information in the brain is a hotspot field of modem neuroscience. This paper attempts to analyze the synaptic connection in both structure and function from Yin-Yang theory. The connections of axons and dendrites between neurons arc malleable and constantly changing, showing a Yin-Yang balance anatomically. Remodeling, stabilization and plasticity changes of synaptic processes also embody the relationship of contradictions, conflicts and transformation of Yin-Yang functionally. Therefore, it is possible to achieve an unexpected result to solve some modem medical problems by using the thoughts and methods of Chinese medicine.

Objective To apply the problem-based learning (PBL) based on the web in the rehabilitation therapy teaching. Methods The 64 students of rehabilitation therapy in grade 2009 and 2010 were taught with selected 3 chapters of physiology, using traditional teaching and PBL based on the web respectively. They were investigated through questionnaire after learning. Results Compared with he traditional teaching, PBL based on the web could improve the interesting of learning, self-study ability, and scope of knowledge. Conclusion PBL based on the web could improve the quality of physiology teaching for students of rehabilitation therapy.

Objective:To explore the influence of family caregiver empowerment intervention model on discharge preparation and quality of life of patients with lung cancer undergoing chemotherapy.Methods:From January 2019 to January 2020, 84 lung cancer patients who received chemotherapy in the Department of Respiratory Medicine in the First Affiliated Hospital of Zhengzhou University were selected, each patient chose one family primary caregiver. It was divided into the control group and the intervention group by the draw method with 42 cases in each group. The control group received routine nursing intervention of internal medicine chemotherapy, and the intervention group received empowerment intervention of main family caregivers on the basis of the control group. The effect of family caregiver empowerment intervention mode were investigated by observing the discharge readiness and quality of life of lung cancer patients.Results:There was no significant difference in the preparation for discharge and quality of life between the two groups before intervention ( P>0.05); after three cycles intervention, the total scores of discharge readiness and quality of life in the intervention group were (76.30±2.80), (94.05±3.70), which were significantly better than those in the control group(73.02±3.73), (87.44±4.18), and the differences were statistically significant ( t values were -4.464, -7.527, P<0.01). Conclusions:Empowerment intervention model of family caregivers can improve the discharge readiness and quality of life of lung cancer patients undergoing chemotherapy.

Nonalcoholic fatty liver disease (NAFLD) is the most common risk factor for diabetes mellitus and cerebrovascular and cardiovascular diseases. The prevalence of NAFLD is increasing rapidly with the improvement in living. Microsome triglyceride transfer protein (MTP) is a key enzyme for outward transport of liver lipids, and the increase in MTP promoter methylation is an important factor for liver lipid deposition in NAFLD. Traditional Chinese medicine believes that “spleen Qi transfers essence”, and the lipid transport function of MTP may be one of the manifestations of “spleen Qi transfers essence”. Clinical studies have shown that the spleen-strengthening and dampness-removing principle is of great importance in the treatment of NAFLD. By reviewing related articles, this article points out that the spleen-strengthening and dampness-removing therapy can improve NAFLD by regulating MTP promoter methylation, increasing the level of hepatic MTP, promoting the outflow of liver lipids, and alleviating lipid deposition.

Objective To investigate whether the effect of transient high glucose on inflammatory factors expression could be continuous in rat glomerular mesangial cell,and its relation with histone methylation modification.Methods Rat glomerular mesangial cells (HBZY-l) were divided into three groups:the high glucose group (25.0 mmol/L glucose),the hypertonic group (MA,5.5 mmol/L glucose+ 19.5 mmol/L mannitol) and the normal-glucose control group (5.5 mmol/L glucose),which were cultured for 24 h respectively.All 3 groups were then changed with normal-glucose medium to culture for 24 h,48 h and 72 h.Their protein,mRNA and supernatant were harvested.The protein expressions of mono-methylation of H3 lysine 4 (H3K4mel) was measured by Western blotting,and the mRNA expressions of NF-κB subunit p65 and set7/9 were determined by real timequantitative PCR.The expression of monocyte chemoattractant protein 1 (MCP-1) and vascular cell adhesion molecule 1 (VCAM-1) were detected by enzyme-linked immunosorbent assay.Results (1)Compared with those in normal control group,the expressions of H3K4mel protein and set7/9 mRNA were first up-regulated in high glucose group,then gradually down-regulated in the following 48 h normal-glucose medium (as compared with those at 0 h,all P ＜ 0.05).At 72 h there was no statistic difference between high glucose group and normal control group (all P ＞ 0.05).(2) Compared with those in normal control group,the up-regulated p65 mRNA,VCAM-1 and MCP-1 sustained at least for 72 h in high glucose group.Conclusions Transient high glucose can induce persistent inflammatory factors expression in rat glomerular mesangial cells,which may via histone modification.

Objective To investigate the expression vibration of microRNA-503(miR-503) and its effect on target gene Bcl-2,caspase enzyme activity and apoptosis of human renal tubular epithelial cells (HK-2) induced by high glucose,and to clarify the pathogenesis of renal tubular injury induced by high glucose.Methods HK-2 cells were cultured in normal glucose group (NG),mannitol hypertonic control group (MA),and high glucose group (HG).The morphology of apoptotic cells was observed using inverted microscope.The expression of miR-503 was determined using realtime quantitative PCR.The apoptosis rate of HK-2 cells was detected by Annexin V-FITC double dye using flow cytometry instrument.The expression of Bcl-2 and cleaved caspase-9 were detected by Western blotting.Results In the high glucose and mannitol groups HK-2 cell,an obviously increased apoptotic rate was observed under inverted microscope compared with normal glucose group (P ＜ 0.05).MA and HG up-regulated miR-503 expression (P ＜ 0.01),down-regulated anti-apoptotic protein Bcl-2 expression (P ＜ 0.05) and up-regulated cleaved caspase-9 (P ＜ 0.05).Conclusions The expression of miR-503 increases in HK-2 cells cultured by high glucose and mannitol.MiR-503 promotes apoptosis of HK-2 cells via activating mitochondrial apoptotic pathways and enhancing cleaved caspase-9 for Bcl-2 insufficiency.The tubular toxicity of high glucose is partly due to osmotic pressure.The miR-503 may be involved in diabetic tubular injury and may be a new therapeutic target of DN.

Objective To observe the expression of microRNA-148b (miR-148b) induced by high glucose in rat mesangial cells,and to explore its effect on its target gene AMP-activated protein kinase α1 (AMPKα1) and extracellular matrix excretion.Methods Rat mesangial cells were divided ino 3 groups:normal glucose (NG,5.5 mmol/L glucose) group,hypertonic (MA,5.5 mmol/L glucose+19.5 mmol/L mannitol) group and high-glucose (HG,25.0 mmol/L glucose) group.MiR-148b expression was detected by real time PCR.Then miR-148b inhibitor was transfected to rat mesangial cells.Their protein expressions of AMPKα1,glucose regulated protein 78 (GRP78),C/EBP homologous protein (CHOP),fibronectin (FN) and collagen Ⅳ were detected by Western blotting.The expression of AMPKα1 mRNA was detected by real time PCR.The expression of collagen Ⅳ was also detected by immunofluorescence.Results Compared with NG group,HG group showed up-regulated miR-148bexpression,down-regulated AMPKαl mRNA and protein expressions,and up-regulated CHOP,GRP78,collagen Ⅳ and FN expressions (all P ＜ 0.05).HG-induced mesangial cells with miR-148binhibitor had up-regulated AMPKα1 mRNA and protein expressions,and down-regulated CHOP,GRP78,collagen Ⅳ,FN expressions as compared with HG-induced cells without miR-148b inhibitor (all P ＜ 0.05).Conclusions HG can up-regulate miR-148b expression and down-regulate AMPKα1 expression in rat mesangial cells,then activate endoplasmic reticulum stress to induce extracellular matrix excretion.MiR-148b inhibitor up-regulates AMPKα1 expression,inhibits endoplasmic reticulum stress and reduces extracellular matrix excretion.

Objective To investigate the expression of Notch signaling molecules, transforming growth factor-β (TGF-β) and fibronectin (FN) in mesangial cell induced by high glucose, and the underlying mechanism of cordyceps sinensis.Methods Rat glomerular mesangial cells were divided into following groups: normal control group (5.5 mmol/L glucose), hypertonic control group (5.5 mmol/L glucose+ 19.5 mmol/L mannitol), high glucose group (25.0 mmol/L glucose), DAPT inhibitor group (25.0 mmol/L glucose + 1 μmol/L DAPT), cordyceps sinensis intervention group (25.0 mmol/L glucose+10 mg/L cordyceps sinensis).Cell proliferation was detected by MTT.The protein and mRNA expression of Notch signaling molecules (Notch1, Jagged1 and Hes1), TGF-β and FN was detected by Western blotting and real time PCR.Results Compared with normal control group, high glucose induced mesangial cell proliferation, as well as the mRNA and protein expression of Notch1, Jagged1, Hes1, TGF-β1 and FN was up-regulated in high glucose group (all P ＜ 0.05).Compared with that in high-glucose group, DAPT and cordyceps sinensis inhibited high glucose-induced mesangial cell proliferation and down-regulated the mRNA and protein expression of Notch pathway, TGF-β1 and FN (all P ＜ 0.05).Conclusion By inhibiting the abnormal activation of Notch signaling pathway and TGF-β signaling pathway, cordyceps sinensis may alleviate high glucose-induced mesangial cell proliferation and reduce extracellular matrix accumulation, thus protecting kidney.

Objective To investigate the underlying mechanism of ursolic acid in attenuating diabetic mesangial cells injury induced by high glucose (HG).Methods Rat glomerular mesangial cells were cultured in normal glucose,HG,HG with LY294002 and HG with ursolic acid.The cell proliferation and hypertrophy were detected by MTT and the ratio of total protein content to cell number.miRNA-21 was detected by quantitative real-time PCR.The PI3K-Akt-mTOR pathway,autophagy associated protein and collagen I were detected by Western blotting and quantitative realtime PCR.The autophagosomes were observed by electron microscope.Results Compared with normal control group,the cells exposed to HG showed up-regulating miRNA-21 expression(P ＜ 0.01),down-regulating PTEN protein and mRNA expression(P ＜ 0.01),up-regulating p85PI3K,phospho(p)-Akt,p-mTOR,p62/SQSTMI,collagen I expressions and down-regulating LC3II expression(P ＜ 0.01).Ursolic acid and LY294002 inhibited HG-induced mesangial cell hypertrophy and proliferation(P < 0.01),down -regulated the expressions of p85Pl3K,p-Akt,p-mTOR,p62/SQSTMI and collagen I and up-regulated the expression of LC3II(P ＜ 0.01).But LY294002 had no effect on the expression of miRNA-21 and PTEN.Ursolic acid down-regulated miRNA-21 expression(P ＜ 0.01),up-regulated PTEN protein and mRNA expression(P ＜ 0.01).Conclusion Ursolic acid may inhibit high glucose-induced mesangial cell miRNA-21 overexpression,up-regulate PTEN,inhibit the activation of PI3K-Akt-mTOR signaling pathway and the enhanced autophagy to reduce the accumulation of extracellular matrix and ameliorate cell hypertrophy and proliferation.