Résumé
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.
Résumé
AIM:To observe protective effect of L-glutamine on myocardial cell injury induced by endotoxin. METHODS:22 male SD rats,weighting(250?30)g,were randomly divided into three groups:control group( n= 7),endotoxin group( n= 7),glutamine/endotoxin group( n= 8). Heart were isolated from rats and perfused on Langendorff apparatus with Krebs- Henseleit(K-H)buffer(Saturation 95%O 2+5%CO 2)at a constant pressure(8.33 kPa)and temperature(37℃). The activity of superoxide dismutase (SOD)and malondialdehyde (MDA)content of efflux from coronary artery, monophasic action potential(MAP)and contractile force were measured at certain timepoints (0 min,20 min,50 min,80 min). RESULTS: Monophasic action potential and contractile force were markedly improved in Gln/ET group. The activity of SOD and MDA level in Gln/ET group restored closely to that in control group. CONCLUSION:L-gluta mine protects myocardial cells from injure induced by endotoxin.
Résumé
?-MSH is an endogenous neuropetide that is effective of all categories of expreimental inflammation. The mechanisms underlying the anti-inflammatory influence of ?-MSH are reviewed in the article. ?-MSH suppresses inflammation in the CNS and periphery by downregulating the activation of NF-?B, then inhibiting production of proinflammatory cytokines, nitric oxide, chemokines and adhension molecules, and increasing synthesis of anti-inflammatory cytokines. ?-MSH is useful in the treatment of many pathological situations in humans.
Résumé
AIM: To further investigate the role of central corticotropin-releasing hormone in stress-induced hyperthermia and lipopolysaccharide (LPS)-induced fever in the rat. METHODS: Test substances were administered intracerebroventricularly (icv) via a third ventricle cannula. Body temperature responses were monitored at 30 min intervals using colonic thermistor probes. Arginine vasopressin (AVP) level in the ventral septal area (VSA) determined by radioimmunoassay. RESULTS: In normal saline controls, rats were handled to take the colonic temperature, their body temperature significantly increased with a peak of (0.88?0.31)℃. The injection (icv) of ?-helical CRH(9-41), a CRH-41 receptor antagonists, markedly attenuated the stress-induced hyperthermia within 90 min after injection of normal saline. LPS(300 ng, icv) stimulated a biphasic rise in the colonic temperature, the 3.5 h thermal response index (TRI 3.5 ) and AVP levels in the VSA of LPS-treated rats were higher than those of control rats. The AVP responses to LPS were inhibited significantly by blockade of central CRH actions using ?-helical CRH(9-41) (5 ?g ,icv) administered 10 min prior to LPS, while ?-helical CRH(9-41) (5 ?g ,icv) resulted in exacerbated febrile responses to LPS(300 ng, icv). CONCLUSION: Central CRH plays an important role in stress-induced hyperthermia. The injection (icv) of ?-helical CRH(9-41) enhances markedly LPS-induced fever in rats. CRH is a dual action molecule in LPS-induced fever, which itself mediates LPS-induced fever, at the same time, and limits the rise in body temperature during fever through actions of AVP in the VSA and glucocoticoids.
Résumé
AIM: To investigate the effect of siduqing decoction,a Chinese medicine,on survival rate and multiple organ dysfunction in mice challenged with LPS. METHODS: Mice were administered intragastrically with Siduqing decoction or distilled water (0.2 ml/10 g) twice a day for 3 days,two hours after Chinese herbal medicine treatment on day 3,LPS or normal saline was injected intraperitoneally,and survival rates in each group were recorded at 12-h intervals. In another experiment,mice were sacrificed at 12 h after LPS,lung,liver,kidney and small intestine were collected and processed for the H & E staining. In addition,Blood was collected at 10 h after LPS injection for determining alanine aminotransferase (ALT) activity,blood urea nitrogen (BUN) and creatinine (Cr) contents. RESULTS: At 96 h after LPS injection,the survival rate (27%, n =34) was lower in LPS group than Siduqing treatment group (65%, n=31,P