This study was aimed to investigate the effects of resveratrol on plasma glucose and the oxidative stress ability in gestational diabetic rats. A total of 100 SD rats with gestation for 5 days were intraperitoneally injected with streptozotocin (STZ, 35 mg?kg-1) to prepare gestational diabetic rat model. Rats were randomly divided into 6 groups, which were the normal gestation group, gestational diabetic model group, resveratrol (30, 60, 120 and 240 mg?kg-1) treatment groups, with 20 rats in each group. A total of 20 rats with gestation for 5 days were selected as the normal gestation control group and another 20 rats with no gestation were selected as the normal control group. The levels of plasma glucose and insulin were determined on 0, 7, 14 days after experiment. Two weeks later, the contents of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) in serum were determined. The results showed that compared with the normal control group, there were no significant difference on the levels of plasma glucose and insulin, the content of MDA, and the activities of SOD, GSH-Px and CAT of the normal gestation control group (P > 0.05). Compared with the gestational diabetic model group, the content of MDA in serum of the resveratrol (30, 60, 120 and 240 mg?kg-1) treatment groups were significantly decreased (P < 0.05,P < 0.01); the level of plasma glucose were significantly decreased and the level of insulin was significantly increased of the resveratrol (120 and 240 mg?kg-1) treatment groups (P < 0.05,P < 0.01); the activities of SOD, GSH-Px and CAT were also significantly increased (P < 0.05, P < 0.01). It was concluded that resveratrol had dose-dependent effect on reducing plasma glucose and improving antioxidant ability in gestational diabetic rats, which perhaps related to its effects on raising the level of insulin and improving the activity of antioxidant enzymes.

A multi-residue analysis method was developed for the determination of 38 kinds of pesticides in nuts (almonds, peanuts, cashew nuts and walnuts) by QuEChERS-ultra-high performance liquid chromatography-tandem mass spectrometry.The pesticide residues were extracted with acetonitrile.The extract was cleaned up with PSA, C18 and Oasis PRiME HLB, and then analyzed by UPLC-MS/MS with multiple reaction monitoring (MRM) mode.External standard method was employed to quantify.The limits of detection (LODs, S/N=3) of this method were between 0.01 and 10 μg/kg, and the limits of quantitation (LOQs, S/N=10) were between 0.05-20 μg/kg.All of the tested pesticides showed good linear relationship (r>0.991).The practical samples were determined at three spiked levels and the average recoveries were between 51.0% and 126.0%.The RSDs were less than 20%.This method was simple, sensitive and accurate, and could be used for the routine analysis of pesticide residues in nuts.

ObjectiveTo investigate the mechanism of dexamethasone (Dex) in inhibiting monocyte adhesion and phagocytose function.Methods Under the stimulation of phorbo1-12-myristate-13-acetate (PMA),U937 monocytes cultured in vitro were treated with Dex and Fasudil respectively.The adhesion rate of U937 monocles to human umbilical vein endothelial cells (HUVECs) and their phagocytic ability of India ink were studied.The protein content and activity of rho-associated coiled-coil protein kinase 1 ( ROCK1 ) as well as the effects of mifepristone and cycloheximide on Dex were determined.ResultsBoth DEX and Fasudil could significantly inhibit the adhesion tate and phagocytosis of U937 cells stimulated by PMA and suppressed the activity of ROCK1.While mifepristone and cycloheximide could not alter these effects of DEX.ConclusionDEX interferes with the adhesion and phagocytosis function of U937 cells by inhibiting ROCKI activity.

Objective To investigate the role of mucosal mast cells infiltration and degranulation with nerve growth factor (NGF)in development of visceral hypersensitivity in Sprague-Dawley (SD)rats. Methods The model of visceral hypersensitivity of irritable bowel syndrome (IBS)was established in 19 neonate SD rats with intestinal stimulation (rectalballon distention)on 8th,10th and 12th postnatal days. The other 19 neonate SD rats without colonic distention were assigned to the control group.After rats grew up (six to eight weeks old),the visceral sensitivity was tested by abdominal withdrawal reflex (AWR)in 10 rats of each group.Mast cell infiltration and degranulation were observed with toluidine blue staining in colon tissue slides.The NGF level of intestinal tissues was detected by enzyme-linked immunosorbent assay (ELISA)methods in the left nine rats of each group.The culture system of dorsal root ganglias (DRG)from the neonatal rats was set up.The changes of electrophysilogical characters of DRG stimulated with NGF (100 ng/mL)for four days were recorded with patch-clamp.Paired t test was performed for comparison between groups.Results The results of AWR indicated that neonatal colonic stimulation could significantly increase visceral sensitivity after growing up.Under 20,40 and 60 mmHg (1 mmHg=0.133 kPa)distention pressure,visceral sensitivity scores of visceral hypersensitivity rats and rats of control group were 1 .00±0.50 vs 1 .67 ±0.50,1 .89 ±0.31 vs 2.89 ±0.34 and 2.89 ±0.33 vs 3.89±0.33,the differences were statistically significant (t=-2.83,-6.00 and -6.00,all P <0.05 ). The results of master cells staining in tissue slides showed colonic master cells infiltration was obvious in rats with visceral hypersensitivity,and part of mast cells were degranulation.The result of ELISA demonstrated that NGF level of visceral hypersensitivity rats was significantly higher than that of control group ((11.07±3.06)pg/mg vs (2.38 ±1.88)pg/mg,t =-6.93,P <0.05).The results of electrophysilogical tests of primary cultured DRG indicated that compared with blank control growp,the action potential threshold of neuron in NGF 100 ng/mL group significantly decreased ((-18.0±2.1 )mV vs (-29.0 ± 2.5 )mV,t = 12.26,P <0.05)and discharge frequency increased ((5 .0± 1 .4 )/800 ms vs (12.0 ± 3.2)/800 ms,t=-8.40,P <0.05 ).Meanwhile,neuron voltage-gated K+ current density remarkably decreased,most were sustained delayed rectifier K+ current (I K )decreasing ((279.0 ±48.0)pA/pF vs (203.0±39.0)pA/pF,t=6.18,P <0.05).Conclusion Colonic stimulation in neonatal rats could cause intestinal master cells infiltration and degranulation,which induced changes of neuron electrophysilogical characters and resulted in visceral hypersensitivity after growing up.

Autism spectrum disorder (ASD) is a multifactorial disease, with social difficulties and repetitive behaviors as its core symptoms. With the improvement of diagnostic methods, the detection rate of ASD is increasing year by year.Cognitive flexibility impairment is very obvious in most autistic patients.More and more studies have shown that cognitive flexibility impairment is related to the occurrence and development of core symptoms. However, the mechanism of cognitive flexibility impairment in autism remains unclear. The frontal lobe plays an important role in advanced cognition, and its complete development is related to cognitive function. Recent studies have shown that frontal lobe dysfunction is closely related to cognitive flexibility deficits in autistic patients, and the abnormal changes in the frontal lobe, the associated default mode network dysfunction and frontal striatal circuit defects may be the important mechanisms of cognitive flexibility impairment. Based on the recent clinical and basic studies on cognitive flexibility in autism, this article reviews the mechanisms of frontal lobe and related circuits involved in the impairment of cognitive flexibility in autism.