ObjectiveTo investigate the effects of Tangmaikang on oxidative and carbonyl stress in streptozocin-induced diabetic rat kidneys,and to also explore their reno- protecting mechanisms in diabetic rats.MethodsRats were randomly divided into three sub-groups:normal control (group A),diabetic control (group B) and diabetic with Tangmaikang (group C).Blood glucose,blood lipid,HbAlC,kidney to body weight ratio and urinary protein excretion were measured after 12 weeks.Malonyldialdehyde (MDA)level,superoxide dismutase (SOD) activity,glutathione peroxidase (GSH-Px) activity,total sulfhydryl group and protein carbonyl levels in renal tissue were also determined.ResultsCompared to group A,kidney to body weight ratio,urinary protein excretion,MDA,and protein carbonyl levels in group B were significantly higher,while SOD and GSH-Px activities and total sulfhydryl group level were significantly lower than those in group A.Kidney to body weight ratio,urinary protein excretion,MDA,and protein carbonyl level in group C were significantly lower than those in group B.SOD and GSH-Px activity in group C were higher than those in group B.ConclusionTangmaikang can prevent renal hypertrophy and decrease urinary protein excretion in diabetic rats.The renoprotective effects of this drug may be related to his ability to inhibit oxidative and carbonyl stress.

Objective To investigate the effects of epalrestat on oxidative and carbonyl stress in streptozocin-induced diabetic rat kidneys, and to also explore their reno -protecting mechanisms in diabetic rats.Methods Rats were randomly divided into three sub-groups:normal control (group A),diabetic con-trol (group B) and diabetic with epalrestat (group C). Blood glucose, blood lipid, HbA1C, kidney to body weight ratio and urinary protein excretion were measured after 12 weeks.Malonyldialdehyde (MDA) level, superoxide dismutase(SOD) activity, glutathione peroxidase (GSH-Px) activity, total sulfhydryl group and protein carbonyl levels in renal tissue were also determined .Results Compared to group A , kidney to body weight ratio , urinary protein excretion , MDA, and protein carbonyl levels in group B were significantly higher , while SOD and GSH-Px activities and total sulfhydryl group level were significantly lower than those in group A.Kidney to body weight ratio , urinary protein excretion , MDA, and protein carbonyl level in group C were significantly lower than those in group B .SOD and GSH-Px activity in group C were higher than those in group B .Conclusion Epalrestat can prevent renal hypertrophy and decrease urinary protein excretion in diabetic rats .The renoprotective effects of this drug may be related to his ability to inhibit oxi-dative and carbonyl stress .

Rat's adrenal medulla(AT group)or adrenal medulla soaked with monosialogan-glioside(AGT group)were transplanted into the head of striatum of rat model of Parkinsonism.Apomorphine induced greater improverment in rotational behavior in AGT group than in AT group with significant difference.Immunocytochemical staining with Chromagranin A showed that a lot of positively stained cells were distributed in the graft area and some cells developed process in AGT group. Our results showed that the monosialoganglioside had effects of increasing the survival of chromaffin cells and inducing the cells to develop processes.

Objective To study the effect of hypothyroidism on oxidative stress status in developing rat brain and to further explore the mechanism of impaired brain development caused by hypothyroidism. Methods Perinatal hypothyroidism was induced by administering propylthiouracil(PTU) solution to the dams by gavage.The oxidative stress indexes were measured in brain homogenate of normal and hypothyroid pups which were sacrificed on the 21st d after birth. Results As compared to the control,the following indexes were found to be increased in the hypothyroid group: protein carbonyl contents,thiobarbital acid reactive substances,reduced glutathione,total antioxidative capacity,activities of superoxide dismutase and glutathione peroxidase(P0.05). Conclusion Hypothyroidism during rat brain development may cause oxidative stress,which may be related to the brain damage caused by hypothyroidism.

Objective To investigate the effects of reactive oxygen species (ROS) inhibition on the down-regulation of adiponectin (ADPN) in mouse 3T3-L1 adipocytes by advanced glycation end-products (AGEs).Methods AGEs were prepared for incubating with cell.3T3-L1 preadipocytes were cultured in vitro and differentiated into mature adipocytes.Cell differentiation and lipid accumulation were determined by oil red O staining.After being intervened with AGEs,2',7'-dichlorofluorescein diacetate (DCFH-DA) was used as a reactive oxygen species (ROS) capture agent and the fluorescent intensity of 2',7 '-dichlorofluorescein (DCF) was detected by flow cytometry.Adiponectin expression under AGEs in 3T3-L1 adipocytes pretreated with N-acetyl-L-cysteine(NAC) or not was detected by real-time fluorescent PCR and ELISA.Results The level of ROS in 3T3-L1 adipocytes treated with AGEs was increased.mRNA and protein of ADPN were down-regulated.After inhibition with ROS,mRNA and protein expressions of ADPN injured by AGEs were ameliorated.Conclusion Exposure of 3T3-L1 adipocytes to AGEs induces oxidative stress in vitro,which decreases the expression of ADPN,and causes functional impairment of adipose cells and insulin resistance.

Objective To investigate the effect of triiodothyronine on the expression of alpha subunit of C protein Co (Coa) gene in cultured rat cerebral cortex neurons. Methods Primary cultured neurons of rat were prepared from the cerebral cortex at embryonic day 19. The neurons were cultured in DMEM supplemented with 15% fetal calf serum. After 7 days, the neurons were cultured in different media; DMEM supplemented with 15% fetal calf serum (group A), DMEM supplemented with 15% fetal calf serum stripped of thyroid hormone (group B), 0.5nmol/L T3-containing DMEM supplemented with 15% fetal calf serum stripped of thyroid hormone (group C) , 5nmol/L T3-containing DMEM supplemented with 15% fetal calf serum stripped of thyroid hormone (group D) and 50nmol/L T3-containing DMEM supplemented with 15% fetal calf serum stripped of thyroid hormone (group E). The neurons were cultured for another 7 days and total RNA was extracted. Goa mRNA leves were measured by competitive RT-PCR. Results As compared with group A, Coa mRNA leves in group B, D and E were low (P 0.05). Conclusion T, has dual effects on the expression of Coa gene in cultured rat cerebral cortex neurons. T3 down-regulated Coa mRNA in cultured neuron. However, in the absence of T3, Goa mRNA was also very low. Thyroid hormone may exert their action on brain development by regulating the the expression of Goa gene.

Acute bulbar palsy is considered an extremely rare manifestation of neuromuscular disorder in thyrotoxicosis.It happens abruptly and progresses quickly,sudden onset of dysphagia is common.It will endanger patient's life without proper treatment.The definite treatment of acute bulbar palsy in hyperthyroidism is to restore the euthyroid state.The dysphagia usually resolves within 3 to 4 weeks.In this article a case of thyrotoxicosis with acute bulbar palsy in reported herewith to call attention to the diagnosis and treatment of this disorder.

Objective To investigate the effects of advanced glycation end products (AGEs) on NADPH oxidase expression in rats′ pancreatic cells. Methods Isets of rats were isolated and intervened with AGEs for certain times (2, 12, 24, 48 h). The Nox2 mRNA expression was assayed by reverse transcription polymerase chain reaction (RT-PCR) and Real-time PCR. NADPH oxidase activity was detected by lucigenin-enhanced chemiluminescence. Results Nox2 mRNA level was 1.75, 2.31-fold higher in AGEs intervened group than control at 12 h and 24 h respectively. The NADPH oxidase activity was increased by AGEs stimulation in a time dependent manner. A distinct peak was at 24 hours and then with a decline , which is still higher than that of the control. Conclusion Exposure of rat islet to AGEs induces NADPH oxidase expression and leads to injury of islet.

Quality control of traditional Chinese medicine (TCM) has become bottlenecks of TCM industry devel-opment and TCM international recognition. To solve the retational problems, we explored the establishment of new quality control method based on efficacy and safety. Firstly, material basis of TCM efficacy was investigated deeply and systematically. Then, quality control method based on efficacy was established by using active ingre-dients as markers. We also establish detection methods based on safety, such as pesticide residues, heavy metals and harmful elements , mycotoxins .

Objective To assess the neuropsychological characteristics in active epileptic patients and investigate itsrisk factors. Methods Ninety adult epileptic patients included 60 active epileptic patients (two or more unprovoked seizures within 12 months) and 30 age-, sex-, education-, course of disease- and seizure type-matched seizure-free subjects (without epileptic seizure for at least 1 year) . The neuropsychological tests including trail making test,digit symbol test, verbal fluency test,digit span test and hamilton depression scale( HAMD) ,were used to detect mental and motor speed, attention, language, working memory and depression symptoms respectively. The neuropsychological tests were compared between active and seizure-free epileptic patients and identified the risk factors of neuropsychological deficits in active epileptic patients. Results Compared to seizure-free subjects, active epileptic patients had significantly worse scores in digit symbol test, verbal fluency test, digit span test ((47.45 ±18. 812) vs(56.40 ±13. 631), (25. 25 ±8. 163) vs(30.40 ±8. 414), (10. 39 ±2. 228) vs( 11. 80 ± 2.074) respectively) ; more time to accomplish the trail making test A and B((64. 35 ±31.710) vs( 45. 47 ± 16. 309) , ( 133. 18 ± 47. 331 ) vs ( 98. 00 ± 35. 003 ) respectively) ; and higher scores in depressive symptoms ((9.12 ±6.219)vs(3.77 ±3.997) ,all P<0.05). Within active epileptic group,significant predictors of neuropsychological deficits were identified in a stepwise linear regression analysis: advancing age was significantly negatively correlated with digit symbol test(β = -0. 468, P = 0. 000) , digit span test (β = -0. 439, P = 0. 000), trail making test A (β =0.365, P = 0.003) and B(β = 0.346, P=0.002) ; higher scores on depressive symptoms was significantly negatively correlated with digit symbol test (β = -0.244, P = 0.015) ; mental work,high-education level and monotherapy were positively correlated with some of the cognitive function subscales. Conclusion This study suggests that active epilepsy can have a direct adverse effect on cognition and depression symptoms. Multi-drug therapy, severity of depression symptoms, advancing age, low-education level and non-mental work are the predictors of neuropsychological impairment in active epilepsy. In addition, good seizure control even after 1 year can have a beneficial impact on cognitive and depression prognosis.