The present study aimed to investigate whether grape seed proanthocyanidin extract (GSPE) has a protective effect on diabetic retinal function. A total of 30 Wistar rats were randomly divided into three equal groups, including the control, diabetic and GSPE-treated diabetic groups. Retinal tissue was harvested and subsequently stained with hematoxylin and eosin. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and methane dicarboxylic aldehyde (MDA) levels were evaluated using respective assay kits; whereas nuclear erythroid 2-related factor 2 (Nrf2) and heme oxygenase (HO)-1 expression levels were assessed by immunohistochemical and western blot analysis. Cell apoptosis in the retina was determined using the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling method. The results showed that the structure of the retina was damaged in diabetic rats, as compared with the control rats. Notably, the structure of the retina improved in the GSPE-treated diabetic group, as compared with the diabetic group. SOD and GSH-Px activities were significantly increased in the retina of rats in the GSPE-treated diabetic group, as compared with the diabetic group (P=0.011 and P=0.001, respectively). Furthermore, a significant reduction in MDA was detected (P=0.013) and the expression levels of Nrf2 and HO-1 in the bladders of rats in the GSPE-treated diabetic group were significantly increased, as compared with the diabetic group (P=0.038 and P=0.043, respectively). Apoptosis of retinal cells was significantly increased in the diabetic group, as compared with the control group (P<0.001); a significant reduction was also detected in the GSPE-treated diabetic group, as compared with the diabetic group (P=0.014). These results demonstrate that GSPE administration may protect the retina against hyperglycemic damage, possibly by ameliorating oxidative stress-mediated injury via the activation of the Nrf2 pathway.

Background Retinoblastoma (RB), depicted as an aggressive eye cancer, mainly occurs in infancy and childhood and is followed by high mortality and poor prognosis. Increasing evidence has revealed that long noncoding RNA taurine upregulated gene 1 (TUG1) is closely linked to the progression of diverse cancers. Nonetheless, the specific function and molecular regulatory mechanism of TUG1 in RB still need to be explored. Methods To explore the specific role of TUG1 in RB. TUG1 expression was detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell counting kit-8 (CCK-8), colony formation, 5-ethynyl-2’-deoxyuridine (EdU), caspase-3, terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) and western blot assays were utilized to study the role of TUG1 in RB. The binding relation between miR-516b-5p and TUG1 or hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase (H6PD) was analyzed by luciferase reporter and RNA immunoprecipitation (RIP) assays. Results The expression of TUG1 was upregulated in RB cells. TUG1 knockdown repressed proliferation ability and promoted apoptosis ability of RB cells. Moreover, TUG1 could bind with miR-516b-5p, which targeted H6PD in RB. In addition, the expression of H6PD was negatively and positively regulated by miR-516b-5p and TUG1 in RB, respectively. Finally, H6PD overexpression could partially offset the effects of TUG1 deficiency on cell proliferation and apoptosis. Conclusions TUG1 promoted the development of RB by sponging miR-516b-5p to upregulate H6PD expression, which might provide a new thought for researching RB-related molecular mechanism.

Meningiomas represent one-third of all primary brain tumors and cause 35,000 new cases each year. Because of this high incidence, we sought to determine if there are proteomic differences between meningiomas and neighboring tissues. Two-dimensional gel electrophoresis and mass spectrometry were used to detect differentially expressed proteins in tumor samples, using arachnoid tissue as a control. Western blot analysis was used to validate the identified candidate proteins. We obtained quantitative data on 112 proteins, 17 of which were down-regulated and 26 of which were up-regulated in meningiomas relative to normal arachnoid tissue. Our analysis showed that the expression of galectin-3, vimentin, and endoplasmin was decreased significantly in meningiomas. The expression of 40S ribosomal protein S12, glutathione S-transferase P, and hypoxia up-regulated protein 1 was increased significantly (P < 0.05). The six above-mentioned differentially expressed proteins might be closely involved with the development of meningiomas. The results of this study provide basic insights into the proteome of meningiomas and provide a preliminary database for further research to enhance understanding of meningioma development.

Expression of miR-34a in cataract rats and its related mechanism were investigated. A total of 30 SD rats were selected and divided into three groups: group A: 2-month-old lucent lens, group B: 18-month-old lucent lens, and group C: 18-month-old naturally occurring cataract lens. The lens was taken and measured by LOC III to determine the degree of lens opacity of the three groups of rats. qPCR was used to detect expression of miR-34a and mRNA of SIRT1 and P53. Western blotting was used to detect the protein expression of SIRT1 and P53. Cell apoptosis was detected by flow cytometry. The lens of rats in group C was more turbid than that of groups A and B (P<0.05). The expression levels of miR-34a and P53 mRNA in the rats lens of group C were significantly higher than those in groups A and B, and the expression of SIRT1 mRNA was significantly lower than that of groups A and group B (P<0.05). Expression of miR-34a in group A was significantly higher than that in group B, the mRNA expression of SIRT1 was significantly lower than that in the lucent lens of 18-month-old rats (P<0.05). The expression of SIRT1 protein in group C was significantly lower than that in groups A and group B, while the expression level of P53 protein in group C was significantly higher than that of groups A and B. The expression of SIRT1 protein in group B was significantly higher than that in group A (P<0.05). The apoptosis rate of group C was higher than that of groups A and group B (P<0.05). In conclusion, the upregulation of expression level of miR-34a is related to cataract occurrence in rats, which may be caused by regulation of SIRT1 protein.