Objective To explore the effect of microRNA-138(miR-138)on injury of ischemia/reperfusion(I/R)induced human renal tubular epithelium(HK-2)cells through neutrophil gelatinase-associated lipocalin(NGAL).Methods HK-2 cells were used to construct I/R model cells,and transfected with miR-138 mimic,miR-138 inhibitor,NGAL,NGAL + miR-138 mimic plasmids,respectively.qRT-PCR determined the expression of miR-138 or NGAL mRNA in different cells to identify the transfection results.Cell counting kit-8(CCK-8)method and flow cytometry were used to detected the activities and apoptosis of cells.ELISA and western blot were used to determine the effects of miR-138 mimic or miR-138 inhibitor on levels of interleukin(IL)-6,IL-1β,tumor necrosis factor(TNF-α)and protein expression of toll like receptor 4(TLR4),nuclear factor kappa-B(NF-κB),inhibitor of NF-κB(IκBα),pho-IκBα(p-IκBα),NGAL of cells.Results miR-138 mRNA expression and cell activity were decreased,while apoptosis increased in I/R cells(P<0.01).Plasmid transfected well,miR-138 mimic increased activity while decreased apoptosis and NGAL mRNA expression of I/R cell.miR-138 inhibitor or NGAL mimic inhibited activity and increased apoptosis and NGAL mRNA expression of I/R cell.The negative effects of NGAL mimic on I/R cell were reversed by miR-138 mimic.miR-138 inhibitor increased levels of IL-6,IL-1β,TNF-α of I/R cell,and increased TLR4,NF-κB,p-IκBα,NGAL protein expression and decreased IκBα protein expression(P<0.05).While miR-138 mimic decreased levels of IL-6,IL-1β,TNF-α of I/R cell,and decreased TLR4,NF-κB,p-IκBα,NGAL protein expression and increased IκBα protein expression(P<0.05).Conclusion miR-138 reduced apoptosis and inflammation factor levels to play a protective role on I/R induced HK-2 cells may through regulating NGAL and TLR4/NF-κB pathway.

Crohn′s disease (CD) is a chronic transmural inflammation disease which may affect the whole gastrointestinal tract. It is known that ileal and colonic involvement of CD is common. Capsule endoscopy (CE) is widely used for CD because of its noninvasiveness and convenience, especially for diagnosis of early-onset and atypical small bowel CD. CE also plays an important role in improving and modifying disease extent and assessment of disease activity. However, CE has its limitations. We mainly summarize the efficacy of CE for early-onset diagnosis and evaluation of extent and activity in small bowel CD. The retention risks are also reviewed to give some references for clinical practice.

Crohn′s disease (CD) is a chronic transmural inflammation disease which may affect the whole gastrointestinal tract. It is known that ileal and colonic involvement of CD is common. Capsule endoscopy (CE) is widely used for CD because of its noninvasiveness and convenience, especially for diagnosis of early-onset and atypical small bowel CD. CE also plays an important role in improving and modifying disease extent and assessment of disease activity. However, CE has its limitations. We mainly summarize the efficacy of CE for early-onset diagnosis and evaluation of extent and activity in small bowel CD. The retention risks are also reviewed to give some references for clinical practice.

Objective: To investigate the effect of curcumin on intestinal mucosal mechanical barrier in rats with non-alcoholic fatty liver disease. Methods: A total of 30 male Sprague-Dawley rats were equally divided into normal control group, model group, and curcumin intervention group. The rats in the model group and the curcumin intervention group were given high-fat feed for 16 weeks, and those in the curcumin intervention group were given curcumin 200 mg/kg/day by gavage once a day after 8 weeks of high-fat feeding. The rats were sacrificed at the end of week 16. A light microscope was used to observe pathological changes in the liver, an electron microscope was used to observe the tight junction of the intestinal mucosa, an automatic biochemical analyzer was used to measure the serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), chromogenic substrate Limulus amebocyte lysate assay was used to measure plasma lipopolysaccharide (LPS) level, spectrophotometric method was used to measure the activity of serum diamine oxidase, ELISA was used to measure the serum level of tumor necrosis factor-α (TNFα), and immunohistochemistry was used to measure the expression of the tight junction protein occludin. One-way ANOVA test and SNK-q test were used for statistical analysis. Results: Under the light microscope, the control group had no hepatocyte steatosis, the model group had significant hepatocyte steatosis and inflammatory cell infiltration, and the curcumin intervention group had reduced hepatocyte steatosis and inflammatory cell infiltration. Under the electron microscope, the control group had a clear and complete structure of the tight junction of the intestinal mucosa and normal structures of mitochondria and endoplasmic reticulum; in the model group, the structure of the tight junction of the intestinal mucosa was destroyed, the intercellular space was widened, the desmosomes had a loose structure, there was edema in some mitochondria, and the endoplasmic reticulum was dilated; the curcumin intervention group had improvements in the structure of tight junction of the intestinal mucosa, intercellular space, edema in the mitochondria, and dilation of the endoplasmic reticulum. Compared with the control group, the model group had significant increases in the serum levels of AST, ALT, DAO, TNFα, and LPS (q = -15.918, -14.402, -33.700, -8.944, and -10.832, P < 0.05); compared with the model group, the curcumin intervention group had significant reductions in the serum levels of AST, ALT, DAO, TNFα, and LPS (q = 10.457, 7.752, 18.802, 5.202, and 4.279, P < 0.05). In the control group, occludin showed a linear distribution along the top of small intestinal mucosal epithelial cells. The model group had a significant reduction in positive staining compared with the control group, and the curcumin intervention group had a significant increase in positive staining compared with the model group. The relative expression of occludin was 0.29±0.03 in the control group, 0.12±0.02 in the model group, and 0.21±0.02 in the curcumin intervention group (P < 0.05). Conclusion Intestinal mucosal mechanical barrier is impaired in rats with NAFLD. Curcumin can reduce such damage, and its mechanism of action may be related to up-regulating the expression of occludin in the intestinal mucosa and reducing the levels of TNFα and LPS.

Objective To explore the effect and mechanism of relaxin on the production of extracellular matrix (ECM) excreted by high glucose stimulated human renal mesangial cells.Methods Cultured human mesangial cells (HMCs) were divided into three groups:(1) normal glucose group (NG,5.5 mmol/L D-glucose),(2) high glucose group (HG,30 mmol/L D-glucose),and (3) high glucose + relaxin group.Cell count kit (CCK8) was used to examine the cell proliferation.The levels of fibronectin and collagen type Ⅳ in the culture supernatants were examined with a solid-phase enzyme-linked immunoadsorbent assay (ELISA);Western blot method was used to detect the expression of α-smooth muscle actin (α-SMA) protein.The transforming growth factor-β1 (TGF-β1) mRNA expression was detected with quantitative polymerase chain reaction (qPCR) method.Results No proliferation and inhibition effects were observed in both normal and high glucose group.Compared to the normal glucose group,the levels of fibronectin,and collagen type Ⅳ increased significantly (57.28 ± 0.59 vs 41.85 ± 0.03,56.52 ± 0.88 vs 33.80 ± 0.24,P ＜ 0.01)after cultured 48 h in high concentration of glucose.Compared to the high glucose group,a significantly decreases of fibronectin and collagen type Ⅳ (47.08 ± 0.03 vs 57.28 ± 0.59,36.16 ± 0.52 vs 56.52 ±0.88,P ＜0.01) were observed in the relaxin treated group.The expressions of α-smooth muscle actin and TGF-β1 were decreased (P ＜0.01).Conclusions Relaxin can suppress the overproduction of ECM excreted by HMC cultured in high ambient glucose,and its mechanism is partly due to the inhibition of TGF-β1.