Objective To investigate the relationship between the changes of blood lipid 4 indexes and lactic acid level with prog‐nosis in children patients with septicopyemia .Methods Ninety‐five children patients with septicopyemia in our hospital from Janu‐ary 2013 to December 2014 were selected ,including 30 death cases(death group and) and 65 survival cases(non‐death group) .To‐tally 60 age‐and gender‐matched healthy children were enrolled as control group .The levels of serum cholesterol (TC) ,triglyceride (TG) ,high density lipoprotein cholesterol (HDL‐C) ,low density lipoprotein cholesterol(LDL‐C) and arterial blood lactate acid (LAC) were measured ,and the results were compared among the three groups .Results The TC and HDL‐C levels in the death group and the non‐death group were lower than those in the control group (P<0 .05) ,the LDL‐C level of the death group was low‐er than that the control group and survival group(P<0 .05) ,while the TG level in the death group and the non‐death group was higher than that in the control group(P<0 .05) ,moreover the TG level in the death group was increased significantly (P<0 .01) . In the excessive inflammation reaction ,the levels of TC ,HDL‐C and LDL‐C were dropped ,which were also decreased with the dis‐ease development ,but the TG level was increased .The LAC level in the death group was higher than that in the control group and the non‐death group ,which in the non‐death group was recovered to the normal level with the disease condition improvement ,while which in the death group was increased with the disease condition progression ,moreover the difference between on 1 d and 3 d had statistical difference(P<0 .05) .Conclusion Monitoring the levels of the blood lipid and lactic acid has an important significance to judge the severity and prognosis in children patients with septicopyemia .

AIM: To investigate the protective effects of berberine against liver injury induced by lipopolysaccharide in mice and the mechanisms underlying its protective effect.METHODS: The male mice were divided randomly into control,berberine group,LPS group and berberine treatment group.Mice were administered intragastrically with distilled water(0.01 mL/g) or(5 g/L) neutral sulfate berberine(0.01 mL/g) once a day for 5 days and injected intraperitoneally with normal saline or LPS(0.02(mL/g),28 mg/kg)at 1 h after gavage on day 5.Blood was collected for determining alanine aminotransferase(ALT) and aspartate aminotransferase(AST) activities,the content of tumor necrosis factors-?(TNF-?) at 10 h and 2 h after LPS or normal saline injection,respectively.Furthermore,the liver tissue was processed,and histological changes and ultrastructure in liver were observed with light and electron microscopy,malondialdehyde(MDA) content and superoxide dismutase(SOD) activity in liver were also detected.RESULTS: Both ALT and AST activities in serum in LPS group were higher than those in control and berberine treatment group.LPS increased the serum TNF-? content at 2 h after injection,which was reversed by berberine pretreatment.The histological examination showed that LPS caused severe hepatic cell edema,degeneration,apoptosis and even necrosis,and ultrastructure observation demonstrated that LPS induced mitochondrial swelling,condensation and margination of chromatin,irregular nuclear envelope in hepatocytes.The above pathological changes produced by LPS were attenuated by berberine pretreatment.Moreover,MDA contents in liver tissue were higher in LPS group than control and berberine treatment group,but there were no significant difference in SOD activity between berberine treatment and LPS group.CONCLUSION: Berberine has a protective effect on LPS-induced liver injury in mice,the mechanisms may be related to its decreasing the production of TNF-?,inhibiting lipid peroxidation and protecting mitochondria.

AIM: To investigate the mechanisms by which berberine attenuates LPS-induced acute lung injury, and provide a new strategy for the treatment of the lung injury due to LPS. METHODS: BALB/c mice were randomly assigned into three groups (control, LPS group, and berberine treatment group). Mice were administered intragastrically with distilled water (0.1 mL/10 g) or neutral sulfate berberine (50 mg/kg) once a day for 3 days, 1 h after intragastrical treatment on day 3, LPS (20 mg/kg) or normal saline was injected intraperitoneally (ip). All animals were sacrificed 12 h after LPS injection, the left lung tissue sections were prepared for histology analysis and the right lung were used to determine the ratio of wet to dry lung tissue weight (W/D). In another experiment, bronchoalveolar lavage fluid (BALF) was collected, and then the total protein content, and the amounts of white blood cells (WBC) and polymorphonuclear neutrophils (PMN) in BALF were determined. Furthermore, the phosphorylation of cytosolic phospholipase A2 (cPLA2) was detected with immunohistochemical analysis by using phospho-cPLA2(Ser505) antibody, and the contents of thromboxane B2 (TXB2) in BALF, malondialdehyde (MDA) in the lungs, and activity of superoxide dismutase (SOD) in lung tissues were also determined.RESULTS: LPS induced acute lung injury, activated cPLA2, and increased TXB2 content in the BALF and MDA level in the lung tissue. The pretreatment with berberine significantly attenuated lung injury, lung edema and protein leakage induced by intraperitoneal injection of LPS. The expression of phospho-cPLA2 in the lung tissues and TXB2 content in the BALF in the berberine treatment group were lower than those in LPS group (P0.05). CONCLUSION: Pretreatment with berberine remarkably reduces the LPS-induced lung injury, which is, at least in part, through inhibiting phosphorylation of cPLA2 and decreasing lipid peroxidation. These findings provide a new strategy for the prevention and treatment of LPS-induced acute lung injury.