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Hippocampal neurons were treated by thrombin and thrombin receptor activating peptides (TRAP). Cell survival rate was decreased in a dose-dependent manner by MTT assay. The numbers of apoptotic cell and apoptotic rate of hippocampal neurons treated by different concentrations of thrombin were increased in a dose-dependent manner by terminal deoxynucleotidyl transferase (TdT) mediated dUTP-biotin nick end-labeling (TUNEL) method and Flow Cytometry. When the concentration of thrombin is 40 U/mL, TUNEL positive cells and apoptotic rate of hippocampal neurons reached peak value, were 27.3±4.0 and (29.333±4.633)%, respectively. Immunocytochemistry assay show that Bcl-2 protein expression was down-regulated and Bax protein expression was up-regulated with the concentration of thrombin increased. TRAP can mimic the effect of thrombin to induce apoptosis on hippocampal neurons. These data demonstrated that thrombin induced hippocampal neuron apoptosis in a dose-dependent manner through activating protease-activated protein-1 (PAR-1). The change in expression of Bcl-2 and Bax was related with the effect of high concentration thrombin induced apoptosis on hippocampal neurons.

In order to investigate the neurotoxicity of lipopolysaccharide (LPS) on the dopaminergic neurons of substantia nigra and the pathogenesis of Parkinson disease, LPS was stereotaxically infused into substantia nigra (SN). At different dosages and different time points with 5 microg LPS, the damage of the dopaminergic neurons in SN was observed by using tyrosine-hydroxylase (TH) immunohistochemical staining. The results showed that 14 days after injection of 0.1 microg to 10 microg LPS into the rat SN, TH-positive (TH+) neurons in the SN were decreased by 5%, 15%, 20%, 45 %, 96% and 99% respectively. After injection of 5 microg LPS, as compared with the control groups, TH+ neurons began to decrease at 3rd day and obviously decrease at 14th day, only 5% of total cells, and almost disappeared 30 days later. The results suggested that LPS could induce the degeneration of dopaminergic neurons in the SN in a dose- and time-dependent manner.

Objective: To observe the characteristics of praxiology of Parkinson disease (PD) rats. Methods: At 1d, 7d, 14d after PD rats’ model were successful; we observed the markers of rotational behavior of Parkinson disease (PD) rats. For example: start time, continuous time, maximum turning, etc. Results: From 1d to 14d, PD rats, start time of the rotational behavior elongated gradually, continuous time shortened by degrees, maximum rotational speed and the number of the rotational behavior were invariable. Conclusions: Improved method of PD is scientific, reliable, and simple. Substantial nigral pathology of PD rats makes the foundation of the rotational behavior. The injury of substantial nigral can be reflected by maximum rotational speed and the number of the rotational behavior of PD rats.

Objective: To evaluate the neuronal toxicical effects induced by levodopa and explore the method in which PD can be treated reasonably with levodopa. Method: The rat models of Parkinson disease (PD) were made by injecting stereotaxically 6-OHDA to right side of the mesencephic ventral tegmental area (VTA) and substantia nigra pars compacta (SNc). The PD rats were treated intraperitoneally with different dosages (10 mg/kg/d, 50 mg/kg/d, 100 mg/kg/d) and different durations (1 d, 3 d, 5 d, 7 d) of levodopa. At the same time, we observed the injury of substantia nigral by the way of treating PD rats with levodopa for 7 days and then stopped for 7 days. In this study, we used TUNEL to detect the injury of substantia nigra by different doses and durations of levodopa. Results: The number of substantia nigral apoptosis was increased with the changes of doses and durations of levodopa. Conclusions: If we use levodopa intermittently or as little as possible, the toxical action of levodopa may be reduced.

Purpose: To investigate the apoptotic mechanism during the pathological process of Parkinson disease (PD) and explore the availability of Ginkgo biloba extract (EGb) to cure PD. Methods: Followed 6-OHDA injection stereotaxically to right side of substantia nigra pars compacta(SNc), at the date of 1, 7,14 and 21, we used biochemical, immunohistochemical, TUNEL and electron microscopic techniques to evaluate the level of apoptosis (TUNEL), monitor the degree of oxidative reaction (MDA.SOD), and to observe the change of ultrastructure of substantia nigra in the experimental PD models of rats (PD group), the EGb treatment group (EGb group) and the control group. Results: Contrast to the Control group, the number of apoptotic neurons and free radical level increased in the PD group and the EGb group, but the PD group surpassed the EGb group (p

Objective: To observe neuronal toxical effect of Levodopa and investigate whether using Levodopa together with EGb is an ideal, workable method to treat Parkinson disease. Methods: In this study, the rat models of Parkinson disease (PD) were made by injecting stereotaxically 6-OHDA to right side of the mesencephic ventral tegmental area (VTA) and substantia nigra pars compacta (SNc). We used rotational behaviour, TUNEL, immunocytochemical, Nissl’s body staining methods to observe the difference between Levodopa (50mg/kg/d×3d, ×5d, ×7d, L-dopa group) and the combination use of Levodopa and EGb (100 mg/kg/d, E-D group). Results: The numbers of apoptosis and rotation, bFGF protein expression in the L-dopa group surpassed those in the E-D group (P

The protective effect and mechanism of diazepam on ischemia neurons during cerebral ischemia and reperfusion were studied. Sixty-three Wistar rats were divided randomly into nine groups: control group (n = 7), ischemia (is) groups including subgroups of is3 h, is3-h/rep1-h, is3-h/rep2-h, is3-h/rep3-h(n = 7 in each group), diazepam treated groups (10 mg/kg, i.p.), including subgroups of is3-h, is3-h/rep1-h, is3-h/rep2-h, is3-h/rep3-h (n = 7 in each group) with Zea longa's animal model of middle cerebral artery occlusion. The comparison between the ischemia group and diazepam-treated group showed that diazepam could obviously decrease the production of glutamate, asparate, MDA and increase the synthesis and release of GABA, SOD and GSH-PX. It was concluded that diazepam exerted its protective effects on neurons through complex mechanisms of regulating the synthesis and release of excitotary/inhibitory amino acids and free radicals.

Serum anticardiolipin antibody (ACA) was measured in 91 patients with cerebral infarction (CI), 42 patients with cerebral hemorrhage (CH) and 30 healthy controls. The results showed that the ACA in CI and CH patients was significantly higher than in controls and IgG-ACA was the most important iso-type. Stroke in ACA positive group tended to be recurrent and of multi-focuses. Positive rate of IgG-ACA reached its peak within the first week after stroke on-set. The results suggested that ACA was an independent risk factor in CI and CH and might be valuable in stroke prediction.

To observe the effects of heterograft of glomus cells of carotid body on hemiparkinsonian rat models, rats with unilateral 6-hydroxydopamine (6-OHDA)-induced lesions of the right dopaminergic neurons of substantia nigra received intrastriatal glomus cells heterograft. Apomorphine-induced rotation was monitored for 30 min at various time points after grafting. The striata were cut and examined for dopamine content by HPLC and for immunohistochemical staining of tyrosine hydroxylase positive neurons (TH+) at the end of the experiments. The results showed that apomorphine-induced rotational behavior was significantly reduced for 12 weeks and the dopamine contents were significantly elevated after grafting (P

The most striking symptom of hypokalemic flabbiness disease is symmetric flaccid paralysis involving both the upper and lower extremities, which is characterized by weaker proximal muscle groups than distal ones and weaker lower extremities than upper ones. Paralysis is associated frequently with symptoms of the alimentary and circulatory system. Laboratory examinations revealed mainly decrease of serum potassium and hypokalemic changes in the electrocardiogram. Abnormal renal tubular function and decrease of CO2-combining power may be observed in some of the patients. Attention should be given to differentiation of this illness from the other hypokalemic paralytic diseases and Guillain-Barre syndrome. The treatment is aimed mainly at administration of potassium in sufficient dosage and concentration as early as possible.

The new disease entity, hypokalemic flabbiness, is an endemic and epidemic hypokalemic paralytic disease found in recent twenty years mainly in certain rural districts in China where cotton is produced. We have carried out extensive investigations and deep-going research work on it for more than ten years. The following preliminary conclusions were drawn: (1) This disease does not belong to the group of well known hypokalemic paralysis of different origins (such as hypokalemic periodic paralysis and Cohn’s disease, etc.). It refers to a new clinical entity which was first discovered and described in China. Up to the present it has not yet been reported in medical literature abroad. (2) Its etiology is very closely related to the gossypol in the raw cotton seed oil usually taken by the inhabitants living in the endemic areas. (3) Pathologically and pathophysiologically, there are evidences of renal tubular damage and renal tubular acidosis, and the loss of body potassium is via kidney. Allergic reaction may presumably take part in the pathogenesis of this disease.