Retinopathy, a major complication of diabetes, often leads to diabetic macular edema which causes adult blindness in many countries. The acetazolamide and topical application of nonsteroidal antiinflammatory drugs (NSAIDs) are helpful in treating macular edema, but their efficacy as therapeutic agent remains to be proved. Glucocorticoids were used to treat the edema caused by brain tumors.1,2) Intravitreal injection of steroids may be used in treating macular edema when oral administration of acetazolamide and topical application of NSAIDs or steroids are not effective.3) Some studies have reported the efficacy and complications of intravitreal triamcinolone acetonide injection and shown the positive results of intravitreal corticosteroid injection. 4,5) However, the exact mechanism of such treatments was not demonstrated and a large-scale, randomized clinical trial was needed to prove their effects.Several lines of evidence suggest that the pathogenesis of diabetic retinopathy is mediated by inflammatory processes, including leukocyte adhesion and the cytokine network. [6][7][8] Retinal vasculature in diabetes is accompanied by inflammatory cell adhesion, which triggers vascular hyperpermeability and pathologic retinal neovascularization. Vascular endothelial growth factor (VEGF) was thought to mediate leukocytes bind to the vasculature, inducing retinal vascular permeability and leukostasis partially through intercellular adhesion molecule-1 (ICAM-1). So, VEGF and ICAM-1 may be two critical factors for diabetes-induced leukostasis and bloodretinal barrier breakdown.The streptozotocin-induced diabetic rat shows many of the early changes in retinal structure and function that are associated with human diabetic retinopathy.9,10) Therefore, in the present experiment, we investigated the effect of dexamethasone on VEGF and ICAM-1 in streptozotocin-diabetic rats. Accumulated leukocytes were counted in vivo by acridine orange leukocyte fluorography, the retinal vascular permeability was measured by the Evans blue assay. The mRNA and protein level of VEGF and ICAM-1 were analyzed with realtime quantitative polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) respectively. We found that intravitreal dexemethasone injection inhibited VEGF and ICAM-1 expression and reduced leukocyte accumulation, vascular permeability in streptozotocin-induced diabetic rats, which may be the underlying mechanisms of its effect. MATERIALS AND METHODS MaterialsThe experiments were carried out in compliance with the guidelines for animal care and use of China and the experimental protocols were approved by the animal ethics committee of Beijing Capital Medical University. Male pigmented Brown-Norway rats (180 g, nϭ72) were purchased from Vitalriver Laboratory Animals Co., Ltd. (Beijing, China). After an overnight fast, some rats received intraperitoneal streptozotocin injection (60 mg/kg; Sigma Chemical, St. Louis, MO, U.S.A.) in 10 mmol/l citrate buffer (pH 4.5) for diabetes induction. Control nondiabetic animals r...

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BackgroundCorn silk contains proteins, vitamins, carbohydrates, Ca, K, Mg and Na salts, fixed and volatile oils, steroids such as sitosterol and stigmasterol, alkaloids, saponins, tannins, and flavonoids. Base on folk remedies, corn silk has been used as an oral antidiabetic agent in China for decades. However, the hypoglycemic activity of it has not yet been understood in terms of modern pharmacological concepts. The purpose of this study is to investigate the effects of corn silk on glycaemic metabolism.MethodsAlloxan and adrenalin induced hyperglycemic mice were used in the study. The effects of corn silk on blood glucose, glycohemoglobin (HbA1c), insulin secretion, damaged pancreatic β-cells, hepatic glycogen and gluconeogenesis in hyperglycemic mice were studied respectively.ResultsAfter the mice were orally administered with corn silk extract, the blood glucose and the HbA1c were significantly decreased in alloxan-induced hyperglycemic mice (p < 0.05, p < 0.01, respectively), while the level of insulin secretionn was markedly elevated in alloxa-induced hyperglycemic mice (p < 0.05). The alloxan-damaged pancreatic β-cells of the mice were partly recovered gradually after the mice were administered with corn silk extract 15 days later. Also, the body weight of the alloxan-induced hyperglycemic mice was increased gradually. However, ascension of blood glucose induced by adrenalin and gluconeogenesis induced by L-alanine were not inhibited by corn silk extract treatment (p > 0.05). Although corn silk extract increased the level of hepatic glycogen in the alloxan-induced hyperglycemic mice, there was no significant difference between them and that of the control group(p > 0.05).ConclusionCorn silk extract markedly reduced hyperglycemia in alloxan-induced diabetic mice. The action of corn silk extract on glycaemic metabolism is not via increasing glycogen and inhibiting gluconeogenesis but through increasing insulin level as well as recovering the injured β-cells. The results suggest that corn silk extract may be used as a hypoglycemic food or medicine for hyperglycemic people in terms of this modern pharmacological study.

The ability to identify strange conspecifics in societies is supported by social memory, which is vital for gregarious animals and humans. The function of hippocampal principal neurons in social memory has been extensively investigated; however, the nonprincipal neuronal mechanism underlying social memory remains unclear. Here, we first observed parallel changes in the ability for social recognition and the number of parvalbumin interneurons (PVIs) in the ventral CA1 (vCA1) after social isolation. Then, using tetanus toxin-mediated neuronal lesion and optogenetic stimulation approaches, we revealed that vCA1-PVIs specifically engaged in the retrieval stage of social memory. Finally, through the in vivo Ca2+ imaging technique, we demonstrated that vCA1-PVIs exhibited higher activities when subjected mice approached a novel mouse than to a familiar one. These results highlight the crucial role of vCA1-PVIs for distinguishing novel conspecifics from other individuals and contribute to our understanding of the neuropathology of mental diseases with social memory deficits.