Protective roles of liraglutide against brain injury of streptozotocin induced diabetic rats.

Our study aimed to explore the impacts of liraglutide on brain dysfunction of type 2 diabetes mellitus. Rats in liraglutide treatment group were diabetic rats further received daily intraperitoneal administration of liraglutide for continuous 6 weeks. Body weight and blood glucose were measured weekly. Vascular structure changes in brain tissues were evaluated by Periodic acid-Schiff (PAS) staining. Angiopoietin-2 (ANG-2), high-mobility group box 1 (HMGB-1), CD105, NeuN, Oligo-2 in brain tissues were measured by immunohistochemistry staining and ANG-2, HMGB-1, and matrix metalloproteinase-9 (MMP-9) were detected by western blotting. Blood glucose levels of rats in diabetic model group were significantly elevated and blood glucose levels of rats in liraglutide treatment group were reduced to comparable levels with control group. PAS staining showed vascular basement membrane of rats in the diabetic model group was thicker than that of the control group. ANG-2, HMGB1 and MMP-9 were up-regulated in the diabetic model group comparing the control group, while down-regulated after treated with liraglutide (p<0.05). NeuN expressions were significantly higher in liraglutide treatment group. Liraglutide may have protective roles against brain injury of streptozotocin induced diabetic rats by inhibiting HMGB1, which further suppressing the MMP-9 and ANG-2.

Early postsurgical lethal outcome due to splenic littoral cell angioma: A case report.

BACKGROUND: Littoral cell angioma (LCA) is a rare benign vascular tumor of the spleen. Given its rarity, standard diagnostic and therapeutic recommendations have yet to be developed for reported cases. Splenectomy is the only method of obtaining a pathological diagnosis and providing treatment to obtain a favorable prognosis. CASE SUMMARY: A 33-year-old female presented with abdominal pain for one month. Computed tomography and ultrasound revealed splenomegaly with multiple lesions and two accessory spleens. The patient underwent laparoscopic total splenectomy and accessory splenectomy, and splenic LCA was confirmed by pathology. Four months after surgery, the patient presented with acute liver failure, was readmitted, rapidly progressed to multiple organ dysfunction syndrome and died. CONCLUSION: Preoperative diagnosis of LCA is challenging. We systematically reviewed online databases to identify the relevant literature and found a close relationship between malignancy and immunodysregulation. When a patient suffers from both splenic tumors and malignancy or immune-related disease, LCA is possible. Due to potential malignancy, total splenectomy (including accessory spleen) and regular follow-up after surgery are recommended. If LCA is diagnosed after surgery, a comprehensive postoperative examination is needed.

LRG1 promotes angiogenesis through upregulating the TGF­ß1 pathway in ischemic rat brain.

Stroke is a life-threatening disease that results in significant disability in the human population. Despite the advances in current stroke therapies, a host of patients do not benefit from the conventional treatments. Thus, more effective therapies are required. It has been previously reported that leucine­rich­α2­glycoprotein 1 (LRG1) is crucial during the formation of new blood vessels in retinal diseases. However, the function of LRG1 in the brain during the neovessel growth process following ischemic stroke has not been fully elucidated and the mechanism underlying its effect on angiogenesis remains unclear. The purpose of the current study was to demonstrate whether LRG1 may promote angiogenesis through the transforming growth factor (TGF)­ß1 signaling pathway in ischemic rat brain following middle cerebral artery occlusion (MCAO). In the present study, the spatial and temporal expression of LRG1, TGF­ß1, vascular endothelial growth factor (VEGF) and angiopoietin­2 (Ang­2) were detected in ischemic rat brain following MCAO using reverse transcription­quantitative polymerase chain reaction (RT­qPCR), western blot analysis and immunohistochemistry. CD34 immunohistochemistry staining was used as an indicator of microvessel density (MVD). The RT­qPCR and western blotting results revealed that the levels of LRG1 and TGF­ß1 mRNA and protein expression were significantly increased as early as 6 and 12 h after MCAO (P<0.05), respectively, peaked at 3 days and persisted at significantly higher level until 14 days, in comparison with the control group. Additionally, VEGF and Ang­2 were also increased following MCAO. Furthermore, the immunohistochemistry results suggested that the MVD was increased following MCAO. In addition, the results also revealed that the percentage of LRG1­positive cells was positively correlated with the percentage of TGF­ß1­positive cells, and the percentage of LRG1­positive and TGF­ß1­positive cells had a positively correlation with the MVD. Taken together, the present study indicated that LRG1 may promote angiogenesis through upregulating the TGF­ß1 signaling pathway in ischemic rat brain following MCAO. This may provide a potential therapeutic target for the treatment of ischemic stroke.