With 28 of new zealand rabbits, following observations were carried out: effects of intravnnous admiaistration of naloxone, an antagonist of opiate receptor, (1) on the biphasie fever induced by endotoxin; (2) on the body temperature of the normal rabbits. The results obtained indicated: the biphasic fever, which was induced by endotoxin at a dose of 5?g/kg was not changed significantly by the pretreatment of naloxone. However, the body temperature of normal rabbit was decreased to-0.46℃ following the administration of naloxone. The authors suggest that the endogenous opioid peptides are not necessary in the pathogenesis of the endotoxin biphasic fever. However, they play probably some role in the maintaining of physiological body temperature of the rabbit.

In order to determine whether the central mediator participates in the mechanism of the EP biphasic fever, the following experiments were carried out: 1. Effect of EP in different doses on the fever pattern; 2. Changes of the cAMP content in CSF and in plasma during the EP biphasic fever. The results obtained demonstrated: 1. After EP were given intravenously in different doses, different fever patterns were produced. 2. The cAMP contents in CSF were increased markedly in every phase of the EP biphasic fever compared with the normal control. These changes of the cAMP content were paralleled and correlated apparently with the body temperature. However, there Were no obvious changes of the cAMP content in plasma during the EP biphasic fever. It demonstrated that cAMP increased in CSF was synthesized and released by CNS for oneself. The authors deduced from above: The wave of body temperature may be related to the changes of cAMP in center during the EP biphasic fever. The fluctuation of cAMP content in the center caused the set-point to move up and down, and further caused the fluctuation of the body temperature and formed the biphasic fever.

Further study of the effect of monosodium glutamate on body temperature using rabbits as experimental model by repeatedly intravenous injection of MSG. The experimental results showed that the body temperature of rabbits were decreased significantly at a time of each day consecutively for three days with medium dose MSG(0.5g/kg/day) However, this effect was disappeared following the fourth administration of MSG a week later, and so did the fifth administration of MSG two weeks later. Those results suggested that the disappearance of decreased body temperature by MSG may be due to tolerance development after MSG was administrated repeatedly. The authors proposed two hypotheses of mechanisms for the development of MSG"tolerance". which would be investigated further.

A Review] The neuroendocrine-immunoregulatory network is fundamental to the maintenance of homeostasis. In this article, the authors present an overview of the role of neuroimmunoregulatory mechanism in the occurance and development of some diseases, which may have important therapeutic implication for the clinics.

Obesity is a severely public health problem the whole society faces, and it is correlated closely with many diseases, such as diabetesⅡ, hypertension, coronary heart disease,gallstone, and so on. Therefore it threatens people's survival quality severely. Obesity is a multiple-factor disease including genetic, metabolic and behavioral factor, and the gene is the main determining factor. With the development of molecular biology technique, people have founded several genes involved in obesity. Among these genes, the research on obese gene is the most profound. The protein leptin is the expression product of the obese gene. This review elucidates the structure, the main biological function, the mechanism of leptin and it's relationship with obesity.

0.05). CONCLUSION: The scent of camphor and perfume bas negative influence on the learning and memory ability in mice. This may be induced by reducing the phosphorylation of CREB protein. While the scent of apple has no effect on learning and memory ability and hippocampal CREB and pCREB expression.

AIM and METHODS: To investigate the antagonistic effects of polymyxin B(PMB) in combination with glycine(Gly) on the pyrogenicity of endotoxin(ET) in rabbits and the LD 50 of PMB in mice. RESULTS: (1)The antagonistic effect of PMB plus Gly was augmented and the optimal combination was PMB(30 000 U) plus Gly(15 mg) to ET(0.01 ?g); (2)The LD 50 of PMB with or without Gly were 8.38?10 4 U/kg and 6.06?10 4 U/kg in mice, respectively. CONCLUSION: The antagonistic effect of PMB plus Gly on ET showed synergnism and this combination could decrease the toxicity of PMB.

AIM: To establish the cell model of hippocampal neurons impaired by the supernatant of microglia conditioned medium (MCM) induced by LPS, and to study the mechanisms of neuron damage and the protection effect of curcumin. METHODS: The microglia were activated and stimulated by LPS at concentration of 5 μg/L. The supernatant of activated MCM was used to stimulate the hippocampal neurons. The morphology of the neurons was observed under light microscope and the survival rate was detected by MTT. The availability of respiration in the hippocampal neurons was determined by detecting the ratio of lactic acid/pyruvic acid, and the expression of 3 types of 1,4,5-inositol triphosphate (IP3R1, IP3R2, IP3R3) was detected by RT-PCR. RESULTS: The hippocampal neurons were damaged severely by the supernatant of activated MCM, and the morphology of the neurons changed significantly. Compared to control group, the ratio of lactic acid/pyruvic acid in MCM group was elevated and the expression levels of IP3R1 and IP3R3 in the hippocampal neurons were significantly increased. The ratio of lactic acid/pyruvic acid and the expression of IP3R1 in curcumin+MCM group were evidently lower than those in MCM group. However, no effect of curcumin on IP3R3 expression was observed, the changes of neural morphology was also ameliorated in curcumin+MCM group. CONCLUSION: Curcumin protects rat hippocampal neurons from damage induced by LPS-induced microglia condition medium.

AIM:Scopolamine blocks cholinergic transmission and impairs learning and memory in mice．The purpose of this study was to evaluate the memory-improving properties of curcumin on scopolamine-induced memory im-pairment in mice．METHODS：The mice of memory impairment were induced by scopolamine．Step down test and Morris water maze test were used to observe the earning and memory ability in curcumin-treated ice．Biochemical assessments of AChE，MDA，and GSH-Px levels in brains were performed．RESULTS：Oral administration of curcumin ignificantly reduced the numbers of step-down rrors(P<0．05)and prolonged the step-down latency induced by scopolamine(P<0．05)．The escape latency time in mice treated with curcumin Was remarkably educed compared to that in scopolamine group by Morris water maze test(P<0．05)．After the platform was removed，the total time that the mice swam in the tar-get quadrant Was also longer in curcumin group than that in model group(P<0．05)．The data also indicated that curcumin significantly inhibited AChE ctivity(P<0．01)and prevented oxidative stress characterized by the significant reduction in MDA content and the significant increase in GSH-Px activities in the brain(P<0．01)．CONCLUSl0N：Curcumin in-duces cognitive improvement by enhancing the function of cholinergic system and its antioxidant activity．

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.