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ABSTRACT: 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.
Molecules 01/2013; 18(4):3825-38. · 2.39 Impact Factor
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ABSTRACT: Rosiglitazone is a peroxisome proliferator-activated receptor (PPAR)-γ agonist. By inhibiting nuclear factor κB (NF-κB), it decreases tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6) and has an anti-inflammatory effect. Endotoxin shock can induce the production of several inflammatory mediators such as TNF-α and IL-6, leading to multiple organ dysfunction and death. We investigated the effects of rosiglitazone (.3 mg/kg, intravenous administration) on the physiologic attributes and cytokine levels in endotoxin shock in conscious rats. Endotoxin shock was induced by intravenous injection of Klebsiella pneumoniae lipopolysaccharides (LPSs; 10 mg/kg) in conscious rats. Mean arterial pressure (MAP) and heart rate (HR) were continuously monitored for 24 hr after LPS administration. Levels of biochemical and cytokine parameters, including glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN), creatinine (Cre), lactic dehydrogenase (LDH), creatine phosphokinase (CPK), glucose, TNF-α, and IL-6 were measured at 0, 1, 3, 6, 12, and 24 hr after sepsis. Endotoxin shock significantly increased blood GOT, GPT, BUN, Cre, LDH, CPK, glucose, TNF-α, and IL-6 levels and HR, while also decreasing MAP. Rosiglitazone diminished the increase in HR, decreased the markers of organ injury (GOT, GPT, BUN, Cre, LDH, CPK, glucose) and inflammatory biomarkers (TNF-α, IL-6), and did not affect MAP after LPS. In conclusion, rosiglitazone ameliorated endotoxin shock-induced markers of organ injury and suppressed the release of TNF-α and IL-6 in conscious rats.
Biological Research for Nursing 01/2011; 13(1):38-43. · 1.28 Impact Factor
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ABSTRACT: Erythropoietin (EPO) has pleiotropic cytoprotective actions. We investigated the effects of EPO on the physiopathology and cytokine levels after haemorrhagic shock (HS) in conscious rats.
Rats received an intravenous injection of 300 U/kg EPO over 10 min followed by HS via withdrawal of 60% of total blood volume from a femoral arterial catheter (6 ml/100 g body weight) over 30 min. Mean arterial pressure (MAP) and heart rate (HR) were monitored continuously for 18 h after the start of blood withdrawal. Levels of biochemical parameters, including haemoglobin, GOT, GPT, BUN, creatinine (Cr), LDH, CPK, and lactate were measured at 30 min before the induction of HS and 0, 1, 3, 6, 9, 12, and 18 h after HS. Cytokine levels, including TNF-alpha and IL-6, in serum were measured at 1, 9, and 18 h after HS. The kidneys, liver, lungs, and small intestine were removed for pathology assessment at 48 h after HS.
HS significantly increased HR, blood GOT, GPT, BUN, Cr, LDH, CPK, lactate, TNF-alpha, and IL-6 levels and decreased haemoglobin and MAP in rats. Pre-treatment with EPO improved survival rate, preserved the MAP, decreased the tachycardia and markers of organ injury, suppressed the release of TNF-alpha and IL-6 after HS in rats.
Pre-treatment with EPO suppresses the release of serum TNF-alpha and IL-6, along with decreasing the levels of markers of organ injury associated with HS, with such actions ameliorating HS-induced organ damage in rats.
Injury 07/2010; 41(7):724-30. · 1.98 Impact Factor
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ABSTRACT: Osteoprotegerin (OPG) is a potent inhibitor of osteoclasts and plays an important role in bone metabolism. Relatively high serum levels of OPG have been observed in postmenopausal women with osteoporosis compared with age-matched controls. No data, however, are available on the relationship between low bone density and serum OPG levels in postmenopausal hemodialysis (HD) patients.
The enrolled subjects included 28 postmenopausal HD patients and 28 age-matched postmenopausal women with normal renal function as controls. Bone mineral density (BMD) was measured by dual energy x-ray absorptiometry (DEXA) in both hips. Low BMD was defined as femoral neck T-score <-2.5. Serum OPG levels were measured using a commercial enzyme-linked immunosorbent assay (ELISA) kit.
Eight of the age-matched postmenopausal controls (28.6%) and 12 of the postmenopausal HD patients (42.9%) had low BMD. There was no statistically significant difference in low BMD between postmenopausal HD patients and age-matched postmenopausal patients (p = 0.263). The serum OPG level was significantly higher in the postmenopausal HD group (p < 0.001). Increased serum OPG (p = 0.017) and decreased serum albumin (p = 0.021) were significantly correlated with low BMD in postmenopausal HD patients. Univariate linear regression analysis showed that serum albumin (r = -0.455, p = 0.015) was negatively correlated, whereas age (r = 0.423, p = 0.025) and the length of time since menopause (r = 0.397, p = 0.036) were positively correlated with the serum OPG level in postmenopausal HD patients. Multivariate forward stepwise linear regression analysis showed that serum OPG (adjusted R(2) = 0.262, p = 0.003) was an independent predictor of low BMD in postmenopausal HD patients and explained 26.2% of the variance.
Serum OPG is associated with low BMD in postmenopausal HD patients.
Journal of Women s Health 03/2010; 19(4):785-90. · 1.57 Impact Factor
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ABSTRACT: Endotoxin shock can induce the production of several inflammatory mediators such as TNF-alpha, IL-6, and IL-1beta, leading to multiple organ dysfunction and death. Erythropoietin (EPO) has been found to interact with its receptor (EPO-R), expressed in a wide variety of non-hematopoietic tissues, to induce a range of pleiotropic cytoprotective actions. We investigated the effects of low doses of EPO (300U/kg, intravenous administration) on the physiopathology and cytokine levels in endotoxin shock in conscious rats. Endotoxin shock was induced by intravenous injection of Escherichia coli lipopolysaccharide (20mg/kg) in conscious rats. Mean arterial pressure (MAP) and heart rate (HR) were continuously monitored for 48h after LPS administration. Levels of biochemical and cytokine parameters, including glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN), creatinine (Cre), lactic dehydrogenase (LDH), and creatine phosphokinase (CPK) were measured at 0, 1, 3, 6, 9, 12, 18, 24, and 48h after sepsis. Serum TNF-alpha, IL-6, and IL-1beta level was measured at 1h after sepsis. Endotoxin shock significantly increased blood GOT, GPT, BUN, Cre, LDH, CPK, TNF-alpha, IL-6, IL-1beta levels, and HR, while it decreased MAP. EPO further increased the markers of organ injury (GOT, GPT, BUN, Cre, LDH, and CPK), inflammatory biomarkers (TNF-alpha, IL-6, and IL-1beta) and did not affect MAP and HR after LPS. EPO disserved endotoxin shock-induced liver, kidney, lung, and small intestine damage in conscious rats. In conclusion, pre-treatment with low doses of EPO increased the release of TNF-alpha, IL-6, and IL-1beta, along with aggravating endotoxin shock-induced markers of organ injury in conscious rats.
Cytokine 12/2009; 49(2):155-62. · 3.02 Impact Factor
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ABSTRACT: Rhabdomyolysis is one of the causes of acute renal failure. Pentobarbital enhances the action of gamma-aminobutyric acid and suppresses the activities of nuclear factor (NF)-kappaB pathways. In this study, we used pentobarbital to study the effects on the glycerol-induced rhabdomyolysis with acute renal failure in conscious rats.
Rhabdomyolysis was induced by intramuscular injection of 10 mL/kg of 50% glycerol in conscious rats. Ten minutes later, the rats received an intravenous injection of pentobarbital (10 mg/kg in 0.5 mL/h normal saline) or normal saline (0.5 mL/h). Biochemical substances, including blood urea nitrogen (BUN), creatinine (Cre), glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and creatine phosphokinase (CPK) were measured at 0 hour, 1 hour, 3 hours, 6 hours, 12 hours, 24 hours, and 48 hours. Rats were killed by decapitation at 48 hours after glycerol administration, and the kidneys were removed immediately for pathological findings and immunohistochemistry.
Intramuscular injection of glycerol significantly increased blood BUN, Cre, GOT, GPT, CPK levels and induced severe histopathologic damage in the kidneys. NF-kappaB and inducible nitric oxide synthase (iNOS) were increased, and E-cadherin was decreased after glycerol administration, as detected by immunohistochemistry in the kidneys. Posttreatment with pentobarbital decreased blood BUN, Cre, GOT, GPT, CPK levels, decreased the markers of kidney injury, and suppressed the release of NF-kappaB and iNOS after rhabdomyolysis.
Posttreatment with pentobarbital suppressed the activities of NF-kappaB and iNOS, decreased BUN, Cre, GOT, GPT, CPK levels, and decreased the markers of kidney injury after rhabdomyolysis. These actions ameliorated rhabdomyolysis-induced acute renal failure in conscious rats.
The Journal of trauma 08/2009; 67(1):132-8. · 2.48 Impact Factor
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ABSTRACT: 1. Propofol is an anti-inflammatory agent commonly used for general anaesthesia and sedation in intensive care unit patients. Haemorrhagic shock (HS) followed by resuscitation can induce the production of several inflammatory mediators, such as tumour necrosis factor (TNF)-a and interleukin (IL)-10, leading to multiple organ dysfunction and death. 2. In the present study, we investigated the effects of treatment with high-dose (10 mg/kg per h) and low-dose (1 mg/kg per h) propofol after HS on the physiopathology and cytokine levels in conscious rats. 3. The experiments were designed to induce HS by withdrawing 40% of total blood volume from a femoral artery catheter (6 mL/100 g bodyweight) over 30 min. Mean arterial pressure (MAP) and heart rate (HR) were monitored continuously for 48 h after the start of blood withdrawal. Levels of biochemical parameters, including glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN), creatinine, creatine phosphokinase (CPK) and lactate dehydrogenase (LDH), were measured 30 min before and 0, 1, 3, 6, 9, 12, 18, 24 and 48 h after the end of the 30 min blood withdrawal period. Serum cytokine levels, including TNF-a and IL-10, were measured at 1, 6, 12, 24 and 48 h after HS. The kidneys, liver, lungs and small intestine were removed for pathological assessment 48 h after HS. 4. In the present study, HS significantly increased blood GOT, GPT, BUN, LDH, CPK, TNF-a and IL-10 levels in conscious rats. Post-treatment with high-dose propofol accentuated systemic hypotension, increased serum TNF-a and IL-10 levels and increased the severity of organ damage after HS. In contrast, post-treatment with low-dose propofol did not affect MAP, but did suppress increased serum levels of the inflammatory cytokines and improved the survival rate after HS, thus protecting rats against HS-induced organ damage. 5. In conclusion, post-treatment with low-dose propofol ameliorated HS-induced markers of organ injury, suppressed the release of TNF-a and IL-10 and protected against HS-induced liver, kidney, lung and small intestine damage in conscious rats. These findings suggest the need to investigate whether low-dose propofol may be beneficial for patients with HS-induced organ damage.
Clinical and Experimental Pharmacology and Physiology 08/2008; 35(7):766-74. · 1.85 Impact Factor
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ABSTRACT: Sepsis is a severe inflammatory disorder that may lead to multiple organ failure. Lipopolysaccharide (LPS) is associated with Gram-negative sepsis and can activate monocytes and macrophages to release pro-inflammatory mediators such as tumor necrosis factor-alpha (TNF-alpha), nitric oxide (NO) and anti-inflammatory mediator such as interleukin-10 (IL-10). In this present study, we used fluvastatin, a HMG-CoA reductase inhibitor, to study its effects upon LPS-induced endotoxic shock in conscious rats.
The experiments were designed that rats received an intravenous injection of 1mg/kg fluvastatin followed 10min later, by an intravenous injection of 10mg/kg Klebsiella pneumoniae LPS, the latter inducing endotoxic shock amongst conscious rats. Subsequently, the levels of certain biochemical variables and cytokines in serum were then measured during the ensuing 48-h period following sepsis. These included total cholesterol (TCH), triglyceride (TG), blood urea nitrogen (BUN), creatinine (Cre), creatine phosphokinase (CPK), lactic dehydrogenase (LDH), aspartate transferase (GOT), alanine transferase (GPT), tumor necrosis factor-alpha, interleukin-10 and nitric oxide.
LPS significantly increased blood TG, BUN, Cre, LDH, CPK, GOT, GPT, TNF-alpha, IL-10 and NO levels but decreased the blood TCH level. Pretreatment of test rats with fluvastatin decreased blood levels of certain markers of organ injury, suppressed the release of TNF-alpha and increased IL-10, and NO levels following LPS treatment. Fluvastatin did not affect the blood TCH and TG level subsequent to the development of sepsis.
Pre-treatment with fluvastatin suppresses the release of plasma TNF-alpha, increases plasma IL-10, and NO production, and decreases the levels of markers of organ injury associated with endotoxic shock, so ameliorating LPS-induced organ damage amongst conscious rats.
Resuscitation 08/2007; 74(1):166-74. · 3.60 Impact Factor
