IntroductionThe aim was to devise an animal model showing some of the neuropathological changes seen in senile dementia, and to investigate the effect of celastrol on cognition neuropathology in this model.Material and methodsForty male Sprague Dawley rats weighing 300–350 g were randomly divided into 5 groups (n = 8 each): control (Con); inhaled sevoflurane (Sev); diabetes mellitus (DM); diabetes mellitus + inhaled sevoflurane (DM/Sev); diabetes + inhaled sevoflurane + celastrol (Cel). Diabetes was induced by an intraperitoneal injection of streptozotocin (STZ). After 20 days, the Sev, DM/Sev and Cel group rats inhaled 3% sevoflurane for 2 h, while the control and DM groups inhaled air. Cel group rats were given intraperitoneal injections of celastrol (0.7 mg/kg) daily for 4 days, while the control group received intraperitoneal injections of an equal volume of dimethylsulfoxide. The Morris water maze test was performed to test cognition. Animals were killed after the last water maze test and Congo red staining was used to observe deposition of amyloid substance in the hippocampus. The expression of GFAP and IGF-1 in the hippocampus was observed by immunohistochemistry.ResultsDiabetes decreased cognition, increased amyloid substance and GFAP expression, and decreased IGF-1 expression in the hippocampus (all p-values < 0.05). Sevoflurane administration intensified and celastrol decreased these changes (all p-values < 0.05).ConclusionsSev/DM rats showed cognitive and neurochemical changes similar to those seen in senile dementia. Celastrol decreased these changes and should be evaluated further as a possible clinical agent in dementia.

The diabetic kidney is sensitive to ischemia-reperfusion (I/R) injury due to microvascular complications, such as cellular apoptosis and necrosis. The aim of this study was to determine if sevoflurane pretreatment could help preserve renal function in rats with diabetes mellitus (DM) by altering non-receptor tyrosine kinases steroid receptor coactivator (Src) and focal adhesion kinase (FAK) expression (Src and FAK are mediators of cellular apoptosis and necrosis). Male rats (N = 40) were randomly assigned to one of five groups: Group A, sham operation; Group B, renal I/R injury; Group C, DM + sham operation; Group D, DM + renal I/R injury; and Group E, DM + sevoflurane pretreatment + renal I/R injury. Sevoflurane pretreatment comprised exposure to 2.5 % sevoflurane for 30 min, followed by exposure to air for 10 min. After 24 h, serum creatinine (Cr) and blood urea nitrogen (BUN) levels, and renal Src and FAK expression (immunohistochemistry) were assessed. Compared with rats in C, rats in D had significantly higher Cr and BUN levels, but significantly lower renal Src and FAK expression. Rats in E had significantly lower serum Cr and BUN levels and significantly higher renal Src and FAK expression levels than rats in D. Our findings suggest that sevoflurane pretreatment in rats with DM protects the kidneys from ischemia/reperfusion injury in part due to increased renal Src and FAK expression.

Aurantio‐obtusin (AUR) is the main bioactive compound among the anthraquinones, from Cassia seed extract. This study was conducted to identify whether AUR could improve obesity and insulin resistance, induced by a high‐fat diet in obese mice. Mice were fed a high‐fat diet for 6 weeks and were then assigned to the high‐fat diet (HFD) control group, the AUR 5 mg/kg group, or the AUR 10 mg/kg group. AUR improves glucose by activating the expression of PI3K, Akt and GLUT4, GLUT2. AUR altered the expression levels of several lipid metabolism‐related and adipokine genes. AUR decreased the mRNA expression of PPAR‐γ, FAS and increased the mRNA expression of PPAR‐α in liver. AUR lowered SREBP‐1c, FAS, SCD‐1, inflammatory cytokines, and increased the expression of PPAR‐γ, PPAR‐α, CPT‐1, and adiponectin in white adipose tissue (WAT). AUR docking with the insulin receptor showed that the residues of the insulin receptor, ectodomain, were the same as those around the emodin. The effect of AUR may be elicited by regulating the activity of the insulin signaling pathway, expression of lipid metabolism‐related genes, and expression of inflammatory cytokine markers to improve adiposity, insulin resistance, and dyslipidemia.

This study demonstrated that DSS has a protective effect on neuroinflammation in LPS-induced BV-2 microglia cells through the TLRs/NF-κB signaling pathway.