0.999,the limits of detection of five ultraviolet absorbents were 4 to 6 mg/L and the minimum detectable concentration was 0.01%-0.015%.The rates of recovery for this method ranged from 98.35% to 102.75% and the relative standard deviations of this method were 0.44% to 1.73%.Conclusion The method is simple,rapid,accurate and applicable to simultaneous determination of the five ultraviolet absorbents in cosmetics.

Objective To compare the differences in responsive ability and oxidative stress damage between type 2 diabetic rats and normal rats under acute sepsis associated with stress hyperglycemia.Methods GK rats with type 2 diabetes and Wistar rats were established critical ill models of sepsis by intraperitoneal injection of 5 mg/kg lipopolysaccharide(LPS).Before and after LPS injection,serum levels of proinflammatory cytokines tumor necrosis factor α (TNF-α),interleukin (IL)-1β3,and IL-6,and anti-inflammatory cytokine IL-10 were determined.Malondialdehyde (MDA) and total antioxidative capacity (T-AOC) levels in serum and tissues (lung,liver,kidney,heart) were measured by colorimetric determination.Results Before LPS injection,serum levels of TNF-α,IL-6,and IL-10 in GK rats were higher than those of Wistar rats.The serum levels of TNF-α,IL-6,and IL-10 after LPS injection were raised in both GK rats and Wistar rats (all P＜0.05).At baseline,serum MDA level of GK rats was higher than that of Wistar group [(25.76 vs 12.71) μmol/L,P＜0.05],while T-AOC level were lower [(0.60 vs 2.8) U/ml,P＜0.05].One hour after LPS injection,the serum MDA level in two kinds of rats significantly increased compared with those of their baseline levels [(32.30 and 20.19) μmol/L,both P＜0.05],while their serum T-AOC level decreased [(0.20 and 2.08) U/ml,P＜0.05]).There were no signigicant differences in the change trend of serum MDA and T-AOC between the two kinds of rats.MDA and T-AOC levels in tissues had no significant difference before and after LPS injection in GK and Wistar rats (P＞0.05).Conclusions The rats with type 2 diabetes had lowered level of proinflammatory factors and raised level of anti-inflammatory factors under acute sepsis,presenting better tolerance and lowered probability of inflammatory diffusion compared with normal rats.

Objective To investigate the glucolipid metabolism in lipoprotein lipase (LPL) gene knockout mice, and to explore the possible mechanisms of insulin resistance. Methods 16- and 40-week old LPL gene knockout heterozygous mice( LPL + / -) and wild type ( WT) C57 mice were selected and divided into 4 groups:16-week LPL+ / -(n=6), 16-week WT(n = 6), 40-week LPL+ / -(n = 6), and 40-week WT(n = 6) group. LPL activity of post-heparin serum was examined. Serum triglyceride( TG) and free fatty acid( FFA) were measuzed. Intraperitoneal glucose tolerance test(IPGTT) in 4 groups of mice were performed. The glucose area under the curve (AUCG) and homeostasis model assessment for insulin resistance index and β-cell function index ( HOMA-IR, HOMA-β) were calculated to evaluate insulin sensitivity and the function of islet β-cells. Serum malondialdehyde (MDA) and total antioxidant capacity ( TAOC) levels were determined by means of colorimetric method. Using dihydroethidium( DHE) fluorescent staining method, reactive oxygen species ( ROS) levels in liver and skeletal muscle were determined. Results LPL activity levels of both 16- and 40-week LPL+ / - mice were significantly lower than that in WT mice of the same age. Serum TG and FFA of 40-week old LPL+ / - mice were significantly higher than those in WT mice of the same age(P<0. 05), and they were also higher than those of 16-week old LPL+ / - mice(P<0. 05). IPGTT showed that compared with WT mice, blood glucose level in LPL+ / - mice was significantly higher than that in WT group at 30 and 120 minute(P<0. 05), and fasting insulin and HOMA-IR were increased significantly(P<0. 05). Serum MDA of 40-week old LPL+ / - mice was evidently higher than that in WT mice by the same week(P<0. 05), while TAOC level was lower than that of WT mice (P<0. 05). ROS in skeletal muscle of 16-week old LPL+ /- mice was significantly increased. Meanwhile, ROS in both liver and skeletal muscle of 40-week old LPL+ / - mice was significantly higher than that in WT mice of the same age. Conclusion As time goes by, lipid and glucose disorders of LPL+ / - mice are aggravating, and insulin resistance develops evidently. Insulin resistance in LPL+ / -mice with dyslipidemia may be related to oxidative stress.

Objective To investigate the effect of fenofibrate on glucolipid metabolism and insulin sensitivity in lipoprotein lipase heterozygous knockout ( LPL+/-) mice, and to explore its mechanism. Methods LPL+/- mice and wild type ( WT) C57 mice were selected and divided into 3 groups ( n=6 each group):LPL+/-( FB) group, LPL+/-(W)group,andWTgroup.MiceinLPL+/-(FB)groupweregavagedwithfenofibrate(50mg·kg-1·d-1)for8 weeks. Mice in LPL+/-( W) and WT groups were orally fed with the same volume water as that in LPL+/-( FB) group for 8 weeks. Body weight was observed. Plasma triglyceride ( TG ) and free fatty acid ( FFA ) were measured. Intraperitoneal glucose tolerance test in 3 groups of mice were performed. The glucose area under the curve ( AUCG) and homeostasis model assessment for insulin resistance index ( HOMA-IR) were calculated. Insulin-stimulated Ser473 Akt phosphorylation in liver and skeletal muscle was measured by Western blot. Reactive oxygen species ( ROS) levels in liver and skeletal muscle were determined by dihydroethidium staining method and superoxide dismutase ( SOD) and catalase ( CAT) mRNA expression levels were detected by real-time PCR. Results Compared with LPL+/-( W) mice, body weight of LPL+/-( FB) mice was lowered, plasma TG and FFA levels were decreased by about 46.0％and 76.5％respectively, and fasting insulin level and HOMA-IR were decreased while there were no significant differences in fasting glucose level and AUCG between two groups. Insulin-stimulated Ser473 Akt phosphorylation levels in liver and skeletal muscle of LPL+/-mice were enhanced by fenofibrate. ROS level in skeletal muscle of LPL+/-( FB) mice was lower than that in LPL+/-( W) mice while there was no significant difference in ROS of liver between two groups. Fenofibrate significantly increased SOD and CAT mRNA expressions in skeletal muscle of LPL+/-mice, but not in liver. Conclusion Fenofibrate reduces body weight, ameliorates lipid metabolism, and improves insulin sensitivity in LPL+/- mice, with reduced oxidative stress.