AIM:To explore the effect of sesamin on blood fat,blood glucose and vascular remodeling in rats fed with high-fat,refined-sugar diet.METHODS:A high-fat,refined-sugar diet was given to rats for 24 weeks.Sesamin(120,60,30 mg?kg-1?d-1)was given by intragastric administration to the rats at 9th week,which lasted for 16 weeks.After 24 weeks,blood glucose,blood fat,blood pressure,activity of total anti-oxidation capacity(T-AOC)and concentration of hydrogen peroxide in serum and aorta were determined.Changes of histology and collagen fibers were observed in aorta by HE and Masson' staining,respectively.Immunohistochemical method was used to examine iNOS protein expression in aorta.In mesenteric arteries,media thickness(M),luminal radius(L)and ratio of media to lumen(M/L)were measured.RESULTS:Compared to model group,sesamin(120,60 mg?kg-1?d-1)obviously decreased the levels of blood glucose,blood fat,blood pressure and concentration of hydrogen peroxide in serum and aorta.Sesamin also markedly enhanced the activity of T-AOC in serum and aorta and reduced collagen deposition and iNOS protein expression in the vascular wall.In addition,proliferation of intima and vascular smooth muscle cells were improved.In mesenteric arteries,sesamin lessened M and M/L and increased L of mesenteric arteries.CONCLUSION:Sesamin ameliorates disorders of glucose and lipid metabolism and inhibits vascular remodeling in rats caused by chronic high-fat,refined-sugar diet.

This study is to observe anti-lipotoxic effect of sesamin on renovascular hypertensive rats fed with a high-fat, high-sucrose diet. Thirty-four complex model rats were induced by two-kidney, one-clip method and on high-fat and refined-carbohydrate diet for thirteen weeks. From the fifth week, intragastric administration of sesamin (120, 60 and 30 mg x kg(-1) x d(-1)) lasted for eight weeks. Blood pressure (BP), blood fat (BF), blood glucose (BG), free fatty acids (FFA), insulin (Ins), tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 were determined. Pathological changes of pancreas, perirenal fat and liver were semiquantitatively analyzed. In sesamin (120 and 60 mg x kg(-1) x d(-1)) group, it was found that there were decrease of levels of BP, BF, BG, TNF-alpha, IL-6 and FFA, improvement of insulin resistance and glucose tolerance, alleviation of body weight, humid weight of fat, liver and pancreas and their organ index, and reduction of islet cell hyperplasia and amount of lipid droplet vacuoles in lipocyte and hepatocyte. It is implied that sesamin had anti-lipotoxic effect and its mechanism may be closely associated with the amelioration of insulin resistance via reducing lipidoses in hepatocyte and inflammatory adipokines such as TNF-alpha and IL-6.

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AIM:To explore the effects of sesamin on blood glucose,blood lipids and vascular cell adhesion molecule-1(VCAM-1)protein expression of aorta in rats with metabolic syndrome.METHODS:A high-fat,refined-carbohydrate diet was given to rats to induce metabolic syndrome for 24 weeks.Sesamin(120,60,30 mg?kg-1?d-1)were given to the metabolic syndrome rats at the ninth week by intragastric administration,which were lasted for 16 weeks.Then,the body weight and abdominal fat of all rats were weighed and the levels of blood lipid,blood glucose,the total anti-oxidation capacity(T-AOC)and the hydrogen peroxide concentration in the serum were determined.In addition,the pathological change and the VCAM-1 protein expression of aorta were observed by H-E staining and immunohistochemical method respectively.RESULTS:Compared with those in model group,the body weight and abdominal fat of sesamin(120,60 mg?kg-1?d-1)groups were obviously decreased,the levels of serum TG,TC,LDL-C and blood glucose were markedly decreased and the level of HDL-C was increased.The VCAM-1 protein expression of aorta was depressed.The pathological change was improved;The T-AOC and hydrogen peroxide concentrations of serum and aorta were decreased.CONCLUSION:Sesamin can obviously descrease the levels of blood lipid,blood glucose and depress the VCAM-1 protein expression of aorta,improve the pathological change of aorta and protect against the progression of atherosclerosis.

Aim To explore renoprotective effect of sesamin in metabolic syndrome rats.Methods Metabolic syndrome was induced by high-fat and refined-carbohydrate diet.Sesamin(120,60 and 30 mg?kg-1?d-1)and simvastatin(5 mg?kg-1?d-1)were given to the metabolic syndrome rats at 9th week,which lasted for 16 weeks.After 24 weeks,body weight,left kidney humid weight,blood sugar,blood fat,systolic blood pressure,renal function,and indexes of oxygenation and antioxygenation for renal cortex were measured.Pathological changes,collagen deposition and iNOS protein and nitrotyrosine expression of kidney were observed by HE-staining,Masson-staining and immunohistochemical method,respectively.Results Decreasein blood sugar,blood fat,blood pressure,and MDA,?OH and NO2-/NO3-in renal cortex was obviously observed in high-and middle-dosage sesamin groups;activities of T-SOD,CAT and GSH-Px in renal cortex was increased;expression of iNOS protein and nitrotyrosine in kidney was down-regulated;inflammatory cell infiltration and collagen deposition in renal glomerulus and renal interstitium were improved;glomerular sclerosis and renal interstitial fibrosis were reversed;renal function was ameliorated.Conclusion Sesamin played a role in antioxidative stress and had protective effect upon renal diseases in metabolic syndrome rats.

AIM: To study the effect of sesamin on expression of inducible nitric oxide synthase(iNOS)and nitrotyrosine(NT)in rat liver tissue with metabolic syndromic hepatic steatosis. METHODS: The rat model of metabolic syndromic hepatic steatosis was induced by operation of two kidneys with one clip(2K1C)and high-fat. The rats taken from that successful model were randomly divided into model group and sesamin(120, 60, and 30 mg·kg~(-1)·d~(-1))groups. In addition, the sham-operated group was set up. The rats in treated group were given sesamin intragastrically everyday for 8 weeks. The levels of blood lipids(TC, TG and FFA)in serum were detected. The activity of SOD and MDA level in the liver homogenate were determined. The expressions of iNOS and NT proteins were detected by Western blotting analysis. The histopathological changes were observed by HE staining in the liver tissues. RESULTS: Compared to model groups, sesamin(120, 60 mg·kg~(-1))significantly inhibited the elevation of serum TC, TG, FFA, and MDA in liver homogenate(P<0.05), and increased the activity of SOD(P<0.05). It also decreased the protein expression of iNOS and NT(P<0.05), and ameliorated the degree of hepatic steatosis. CONCLUSION: Sesamin prevents and cures the metabolic syndromic hepatic steatosis. The mechanism is probably mediated through decreasing the protein expression of iNOS and NT, and alleviating the oxidative stress in addition to regulating the lipid metabolism.

The aim of the present study is to investigate the protective effect of chrysin (5,7-dihydroxyflavone) on right ventricular remodeling in a rat model of monocrotaline-induced pulmonary arterial hypertension (PAH). PAH rats were induced by a single injection of monocrotaline (60 mg x kg(-1), sc) and were administered with chrysin (50 or 100 mg x kg(-1) x d(-1)) for 4 weeks. At the end of experiment, the right ventricular systolic pressure (RVSP) and mean pulmonary artery pressure (mPAP) were monitored via the right jugular vein catheterization into the right ventricle. Right ventricle (RV) to left ventricle (LV) + septum (S) and RV to tibial length were calculated. Right ventricular morphological change was observed by HE staining. Masson's trichrome stain was used to demonstrate collagen deposition. The total antioxidative capacity (T-AOC) and malondialdehyde (MDA) levels in right ventricle were determined according to the manufacturer's instructions. The expressions of collagen I, collagen III, NADPH oxidase 4 (NOX4) and nuclear factor-kappa B (NF-κB) were analyzed by immunohistochemisty, qPCR and (or) Western blot. The results showed that chrysin treatment for 4 weeks attenuated RVSP, mPAP and right ventricular remodeling index (RV/LV+S and RV/Tibial length) of PAH rats induced by monocrotaline. Furthermore, monocrotaline-induced right ventricular collagen accumulation and collagen I and collagen III expression were both significantly suppressed by chrysin. The expressions of NOX4, NF-κB and MDA contents were obviously decreased, while the T-AOC was significantly increased in right ventricule from PAH rats with chrysin treatment. These results suggest that chrysin ameliorates right ventricular remodeling of PAH induced by monocrotaline in rats through its down-regulating of NOX4 expression and antioxidant activity, and inhibiting NF-κB expression and collagen accumulation.

Crocetin, a naturally occurring carotenoid, possesses antioxidant and antiatherosclerotic properties, of which the underlying mechanism remains unclear. In the present study, we examined the effects of crocetin (0.1, 1, 10 μmol·L(-1)) on angiotensin II (Ang II, 0.1 μmol·L(-1)) induced expression of vascular cell adhesion molecule-1 (VCAM-1) in human umbilical vein endothelial cells (HUVECs) and monocyte-endothelial cell adhesion. The effects of crocetin on the activation of nuclear factor kappa B (NF-κB) and intracellular reactive oxygen species (ROS) were also observed. The results demonstrated that crocetin notably suppressed Ang II induced NF-κB activation (P<0.01) and VCAM-1 expression (P<0.05, P<0.01) in HUVECs, accompanied by a markedly reduced monocyte-endothelial cell adhesion (P<0.05, P<0.01). In addition, preincubation with crocetin resulted in a significant enhancement of cellular antioxidant capacity (P<0.05, P<0.01), while Ang II induced intracellular ROS decreased markedly (P<0.05, P<0.01). These results indicated that crocetin was capable of suppressing Ang II induced VCAM-1 expression and monocyte-endothelial cell adhesion by suppression of NF-κB activation, which might be derived from the enhancement of antioxidant capacity and subsequent reduction of intracellular ROS.

The parabrachial nucleus (PB)is made up of gray matter around the Pons combination(BC),mainly consisting of glutamatergic,GABAergic and enkephalinergic neurons.PB is connected to hypothalamus and basal forebrain through a network of nerve fibers.Specific lesion of the entire parabrachial complex in animals leads to a deep coma.PB also projects to the non-rapid eye movement(NREM)-related regions including the ven-trolateral preoptic,and receives the projections from the parafa-cial zone.Activation of the GABAergic neurons in parafacial zone can promote NREM sleep,which indicates that PB partici-pates in NREM sleep.Furthermore,the lateral PB is actived when rapid eye movement(REM)sleep is deprived.In conclu-sion,PB participates in regulating wakefulness, NREM and REM sleep.This review summarizes the advances in the roles of PB in sleep-wake regulation.

The aim of the present study is to investigate the effects of sequoyitol (Seq) on expression of eNOS and NOX4 in aortas of type 2 diabetic rats. Type 2 diabetic rats induced by high fat and high sugar diet and low dose of streptozotocin (STZ, 35 mg x kg(-1)) and were administered Seq (12.5, 25 and 50 mg x kg(-1) x d(-1)) for 6 weeks. The fasting blood glucose (FBG) and body weight were tested. Acetylcholine (Ach) induced endothelium-dependent relaxation and sodium nitroprusside (SNP) induced endothelium-independent relaxation were measured in aortas for estimating endothelial function. Aortic morphological change was observed with HE staining. The level of serum insulin was measured by radioimmunoassay. The total antioxidative capacity (T-AOC), malondialdehyde (MDA) and NO levels in aortas were determined according to the manufacturer's instructions. In addition, the expressions of eNOS and NOX4 in aortas were measured by immunohistochemisty, real-time PCR or Western blotting. The results showed that Seq significantly decreased FBG and insulin resistance, and improved aortic endothelium-dependent vasorelaxation function. The expressions of NOX4 and MDA content were obviously decreased, while the expression of eNOS, the levels of NO and T-AOC increased significantly in aortas of diabetic rats with Seq treatment. In conclusion, Seq protects against aortic endothelial dysfunction of type 2 diabetic rats through down-regulating expression of NOX4 and up-regulating eNOS expression.