The potent anti-inflammatory activities and tissue-protective effects of freshwater clams (Corbicula fluminea) have been well reported. The aim of this study was to determine the effects of freshwater clam extract (FCE) supplementation on time to exhaustion, muscle damage, pro- and anti-inflammatory cytokines, and liver injury in rats after exhaustive exercise. Thirty-two rats were divided into four groups: sedentary control (SC); SC group with FCE supplementation (SC+FCE); exhaustive exercise (E); and E group with FCE supplementation (E+FCE). The SC+FCE and E+FCE groups were treated with gavage administration of 20 mg/kg for seven consecutive days. Blood samples were collected for the evaluation of biochemical parameters. The cytokine levels of TNF-α and IL-10 were also examined. Twenty-four hours after exhaustive exercise, the rat livers were removed for H & E staining. The FCE supplementation could extend the time to exhaustion in exercised rats. The levels of CPK, LDH, AST, ALT, lactate, TNF-α and H & E stains of the liver injury were significantly decreased in the E+FCE group, but the blood glucose and IL-10 were significantly higher in comparison with the E group. This study suggests that FCE supplementation may improve endurance performance and reduce exercise-induced muscle damage, inflammatory stress and liver injury.

1. In the present study, we used a low dose of propofol (5 mg/kg per h) to investigate its effects on the pro-inflammatory cytokines (tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta and IL-10) and changes in nitric oxide (NO) following lipopolysaccharide (LPS) for a period of 12 h in conscious rats. 2. Experiments were designed to induce endotoxin shock by intravenous injection of Klebsiella pneumoniae LPS (10 mg/kg) in conscious rats. Arterial pressure (AP) and heart rate (HR) were monitored continuously for 12 h after LPS administration. Tumour necrosis factor-alpha, IL-1beta, IL-10 and plasma nitrates/nitrites were determined before and 0.5, 1, 3, 6, 9 and 12 h after LPS administration. A low dose of intravenous propofol (5 mg/kg per h) was administered to investigate the effects on cytokine responses and changes in NO in endotoxin shock. 3. Lipopolysaccharide significantly increased TNF-alpha, IL-1beta, IL-10, nitrites/nitrates and HR, whereas mean AP was decreased. Post-treatment with propofol suppressed the release of TNF-alpha, IL-1beta, IL-10 and NO production after endotoxin shock. 4. Lipopolysaccharide also caused a decrease in the white blood cell count and haematocrit. 5. Post-treatment with propofol slightly, but not significantly, affected the LPS-induced systemic hypotension, tachycardia, leukocytopenia and anaemia. 6. These findings suggest that low-dose propofol may be beneficial to the inflammatory change in sepsis.

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SummaryHemorrhagic shock is a common cause of death in emergency rooms. Current animal models of hemorrhage encounter a major problem that the volume and the rate of blood loss cannot be controlled. In addition, the use of anesthesia obscures physiological responses. Our experiments were designed to establish an animal model based on the clinical situation for studying hemorrhagic shock. Hemorrhagic shock was induced by withdrawing blood from a femoral arterial catheter. The blood volume withdrawn was 40% of the total blood volume for group 1 and 30% for group 2 and 3. Group 3 was anesthetized with sodium pentobarbital (25 mg/kg, i.v.) at the beginning of blood withdrawal. Our data showed that the survival rate was 87.5% at 48 h in the conscious group and 0% at 9 h in anesthetic group after hemorrhage. The levels of mean arterial pressure, heart rate, white blood count, TNF-a, IL1-b, CPK, and LDH after blood withdrawal in the anesthetic group were generally lower than those in conscious groups. These results indicated that anesthetics significantly affected the physiology of experimental animals. The conscious, unrestrained and cumulative volume-controlled hemorrhagic shock model was a good experimental model to investigate the physical phenomenon without anesthetic interfernce.

Lipopolysaccharide is strongly associated with septic shock, leading to multiple organ failure. It can activate monocytes and macrophages to release proinflammatory mediators such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and nitric oxide (NO). The present experiments were designed to induce endotoxin shock by an intravenous injection of Klebsiella pneumoniae lipopolysaccharide (LPS, 10 mg/kg) in conscious rats. Arterial pressure and heart rate (HR) were continuously monitored for 48 h after LPS administration. N-Acetylcysteine was used to study its effects on organ damage. Biochemical substances were measured to reflect organ functions. Biochemical factors included blood urea nitrogen (BUN), creatinine (Cre), lactic dehydrogenase (LDH), creatine phosphokinase (CPK), aspartate transferase (GOT), alanine transferase (GPT), TNF-alpha, IL-1 beta, methyl guanidine (MG), and nitrites/nitrates. LPS caused significant increases in blood BUN, Cre, LDH, CPK, GOT, GPT, TNF-alpha, IL-1 beta, MG levels, and HR, as well as a decrease in mean arterial pressure and an elevation of nitrites/nitrates. N-Acetylcysteine suppressed the release of TNF-alpha, IL-1 beta, and MG, but enhanced NO production. These actions ameliorate LPS-induced organ damage in conscious rats. The beneficial effects may suggest a potential chemopreventive effect of this compound in sepsis prevention and treatment.