OBJECTIVE:To investigate the effects of pravastatin on serum levels of CRP and TNF-? in patients with diabetic nephropathy and study its possible mechanism in the treatment of diabetic nephropathy. METHODS:28 patients with diabetic nephropathy were treated with provastatin plus routine therapy (trial group),another 28 patients with diabetic nephropathy were treated with routine therapy alone (control group). Serum levels of CRP and TNF-? in the two groups were detected after treatment for 24 weeks. RESULTS:The total effect rate in the trial group was 67.9% versus 42.9% in the control group(P

Objective: To explore the effect of KangXin oral solution on brain mitochondrial DNA(mtDNA) deletion mutation in aged Balb/c mice.Methods: The Balb/c mice were divided into the young group(6weeks),middle-aged group(6months) and aged group(14 months),each group has 10 mice.Brain mtDNA were obtained and polymerase chain reaction(PCR) technique was used to examine the fragment deletion of brain mtDNA,thus,to confi rm there was deletion of mtDNA in aged mice,s brain.The aged Balb/c mice were divided into two groups: the aged blank control group being given 0.9% normal sodium,KangXin oral solution group.After being treated for four months,the brain mtDNA were obtained and polymerase chain reaction(PCR) technique was used to amplify wild-type and deletion from of mtDNA.Gel imaging meter was used to detect optical density,then,to compare the optical density ratios of deletion from mtDNA/ wide type mtDNA in two groups.Results: There were 304bp mtDNA deletion in brain mitochondrial of aged Balb/c mice,but same mtDNA deletions were not detected in brain mitochondrial of young and middle-aged mice.Compared with aged blank control group,the mtDNA deletion of aged Balb/c mice in KangXin oral solution group decreased obviously(P〈0.001).Conclusion: mtDNA deletion mutation accumulates with the increase of age.KangXin oral solution can inhibit mtDNA deletion of aged mice.

ObjectiveTo investigate the therapeutic effectiveness of defibrase in treating penumbra and reperfusion.MethodsIntraluminal suture method was used to develope reversible middle cerebral artery occlusion(MCAO). Rats were subjected to MCAO 3 hours followed by reperfusion for 3, 6, 24, 72 hours, and to MCAO 6 hours followed by reperfusion for 3, 6, 24 hours. The treatment groups rats were injected intravenously defibrase at 0.5 hour before reperfusion. Meanwhile, the control group received normal saline. Clinically Neurological Deficits Scale were evaluated every day. Infarction volume was measured by using 2,3,5-triphenyltetrazolium chloride staining. Pathologic change were examined microscopically in HE stained sections.ResultsThere were significant difference at treatment groups of reperfusion 3 hours after MCAO.Infarction volume and Clinically Neurological Deficits Scale was significant reduced as control group (P<0.05). There were no significant differences at treatment groups of reperfusion 6 hours after MCAO (P>0.05). Cerebral hemorrhage wasn't increased in defibrase treatment group.ConclusionsDefibrase was effective on Clinically Neurological Deficits of rats in reperfusion 3 hours after MCAO.

Acupuncture Points ; Adult ; Female ; Humans ; Male ; Meridians ; Radiculopathy ; diagnosis ; therapy ; Spondylosis ; diagnosis ; therapy

AIM: To investigate the influence of Buxinqi Capsule (BXQ) on myocardial ischemia reperfusion injury in rats. METHODS: In this study, the experimental model was established by reperfusion for 60 minutes in rats after ligaturing left anterior descending coronary artery (LAD) for 30 minutes. Serum creatine phosphokinase (CPK), lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyodebis (MDA), area of myocardial infarction and occurrence of arrhymia were investigated. RESULTS: BXQ significantly decreased level of CPK and LDH and MDA, and obviously improved the activity of SOD, decreased reperfusion arrhythmias and arrhythmias severity index (ASI), and decreased the area of myocardial infarction. CONCLUSION: BXQ has protective effect on the damage of myocardia ischemia reperfusion in rats

ObjectiveTo observe the effect of Buzhongyiqi decoction on post stroke fatigue.Methods60 stroke patients with fatigue were given Buzhongyiqi decoction for 4 weeks continuously. Chinese New Drug Clinical Guidelines was to evaluate the effect for patients according to improvement of symptoms.ResultsIn 60 cases, markedly effective in 47 cases (78.33%), effective in 10 patients (16.67%), invalid in 3 cases (5%). Symptoms of malaise, anorexia, muscle soreness were significantly improved.ConclusionBuzhongyiqi decoction can improve post stroke fatigue of stroke patients.

ObjectiveTo observe the effect of digital auditory activation and touching intervention on infants with cerebral dysfunction.Methods388 infants with perinatal high-risk factors and abnormal result of Denver Development Screening Test (DDST) were randomly divided into group A (n=135), group B (n=128) and group C (n=125), and treated with digital auditory activation combined with touching (group A), simple touching (group B) and simple drug (group C) with 10 days as a course. All infants were tested with DDST after one therapeutic course, and tested again with DDST after the infants of group B and group C treated continuously for six therapeutic courses; and all infants were assessed with the Gesell development quotient (DQ) after six months.ResultsAfter one therapeutic course, normal rate of DDST was 71.11% in group A, 26.69% in group B and 20.00% in group C. After six therapeutic courses, that was 90.37 % in group A, 62.50 in group B and 40.00% in group C. After six months, the children with the Gesell DQ over 86 scores was 125 (92.60%) in group A, 90 (70.31%) in group B and 62 (49.60%) in group C. There were significant differences among three groups ( P<0.01).ConclusionThe digital auditory activation combined with touching has short therapeutic course and high efficacy, so it is a good therapeutic method for infants with cerebral dysfunction.

OBJECTIVETo explore the effects of the simultaneous activation of liver X receptor (LXR) and peroxisome proliferator-activated receptor alpha (PPARalpha) on bile acid biosynthesis in rats.

METHODSTotally 36 male SD rats were divided into three groups with 12 rats in each group: control group, high cholesterol (HC) group, and high cholesterol + fenofibrate (HC + FENO) group. Total bile acids (serum bile acids plus fecal bile acids) level was assayed. The levels of mRNA for peroxisomal palmitoyl-CoA oxidase (Acox1), LXR, cholesterol 7alpha-hydroxylase (CYP7A1), D-bifunctional protein (DBP), trihydroxycoprostanoyl-CoA oxidase (Acox2), sterol 12alpha-hydroxylase (CYP8B1), and sterol 27-hydroxylase (CYP27A1) in liver were detected by RT-PCR.

RESULTSTotal bile acid level was significantly higher in HC + FENO group than in HC group (P < 0.01), and both were significantly higher than that in control group (P < 0.01). Compared with HC group, the mRNA expression of Acox1 and DBP was significantly higher in HC + FENO group (P < 0.01), but no statistical differences was found between HC group and control group. The mRNA levels of LXR and CYP7A1 in HC + FENO group and HC group were not significantly different but were both significantly higher than that in control group (P < 0.01, P < 0.05). No changes were observed in Acox2, CYPSB1, and CYP27A1 mRNA levels among these three groups.

CONCLUSIONSimultaneous activation of LXR and PPARalpha can increase of CYP7A1 and DBP mRNA exDression and thus accelerates the biosynthesis of bile acid.

Animals ; Bile Acids and Salts ; biosynthesis ; Cholesterol ; pharmacology ; Fenofibrate ; pharmacology ; Hypolipidemic Agents ; pharmacology ; Liver ; drug effects ; enzymology ; Liver X Receptors ; Male ; Orphan Nuclear Receptors ; agonists ; PPAR alpha ; agonists ; Rats

OBJECTIVETo determine the physiological role of D-bifunctional protein (DBP) in bile acid biosynthesis through investigating the effect of increasing activity of DBP on bile acid biosynthesis.

METHODSTwenty male Wistar rats were divided into two groups: diethylhexyl phthalate (DEHP) group (n = 10) and control group (n = 10). Serum triglyceride, total cholesterol, hepatic DBP activity, and fecal bile acids were assayed. The mRNA levels of hepatic peroxisome proliferator-activated receptor alpha (PPARalpha), DBP, and cholesterol 7alpha-hydroxylase (CYP7A1) were detected by RT-PCR.

RESULTSCompared with control group, serum triglyceride level was decreased significantly and PPARalphamRNA level was increased significantly in DEHP group (P < 0.01). Together with a sharp induction of DBP mRNA expression and DBP activity in DEHP group (P < 0.01), the levels of CYP7A1 mRNA and fecal bile acids were significantly increased by 1.9 times and 1.6 times respectively compared to control group (P < 0.01). There was a significantly positive correlation between DBP mRNA level or DBP activity and CYP7A1 mRNA level (r = 0.89, P < 0.01; r = 0.95, P < 0.01).

CONCLUSIONThe up-regulation of DBP mRNA and activity in liver can result in the increase in CYP7A1 mRNA expression and bile acid biosynthesis, suggesting that DBP may be involved in bile acid biosynthesis together with CYP7A1.

17-Hydroxysteroid Dehydrogenases ; metabolism ; Animals ; Bile Acids and Salts ; biosynthesis ; Cholesterol 7-alpha-Hydroxylase ; analysis ; Enoyl-CoA Hydratase ; metabolism ; Liver ; metabolism ; Male ; Multienzyme Complexes ; metabolism ; PPAR alpha ; analysis ; Peroxisomal Multifunctional Protein-2 ; RNA, Messenger ; analysis ; Random Allocation ; Rats ; Rats, Wistar

BACKGROUND: Acute pulmonary embolism (APE) is a disorder involving the pulmonary circulation resulting from a blockage of the pulmonary artery. The present study aimed to investigate the effects of aspirin on the nuclear factor-κB (NF-κB) activity in a rat model of APE. METHODS: A total of 108 healthy male Sprague-Dawley rats were randomly assigned into six groups (n=18 rats per group): control group, sham operation group, APE model group, and low-, medium- and high-dose aspirin groups. Six, 24, and 72 hours after the induction of APE, rats in the low-, medium- and high-dose aspirin groups were given aspirin at a respective daily dose of 150, 300, and 600 mg/kg by gavage for three consecutive days. Rats in the other groups were treated with equal volumes of normal saline. Six rats in each group were anesthetized with 10％ chloral hydrate solution at each time point, and then the lung tissues were colected and analyzed using immunohistochemical staining. RESULTS: Positive immunohistochemical staining was present in the bronchial epithelial cells, alveolar cells, macrophages, and surrounding bronchial smooth muscle cells. When compared with the APE model group, the number of positive cells was significantly lower in the other groups at each time point (P<0.001). Statistically significant differences were also observed among the aspirin-treated groups at 6 hours (P<0.05,P<0.001). Compared with the APE model group, NF-κB protein expression was reduced in the other groups at each time point (P<0.05,P<0.001). Rats from the APE model group had thrombosis, damaged alveolar walls, and pulmonary hemorrhage, along with different degrees of infl ammatory cellular infiltration at each time point. However, pathological changes such as pulmonary hemorrhage and infiltration of inflammatory cells were attenuated after the aspirin treatment. CONCLUSION: Aspirin can significantly inhibit NF-κB activity in the lung of rats with APE in a dose-dependent manner, and can alleviate lung injury after APE.