Research of Cistanche glycoside on Vascular Dementia

For more information:ali.ma@wecistanche.com

Yang Bo; Liu Shuyan

Keywords: Cistanche glycoside; vascular dementia; cerebral ischemia injury

1. Introduction

1.1 Cases/patients Selection

70 hospitalized patients in our department from March 2008 to April 2010 were randomly divided into the Cistanche glycoside treatment group and the Control group.

Treatment group: There were 37 dementia patients in the treatment group, including 20 males and 17 female patients; aged 55-81 years old, with an average of 72 years old. 29 out of the 37 patients are with cerebral infarction and the rest 8 cases are of a cerebral hemorrhage.

Control group: There were 18 males and 15 female dementia patients; aged 53-82 years old, with an average age of 73 years old. There are 23 patients in the control group with cerebral infarction and 10 patients in the control group with cerebral hemorrhage.

All patients were asked for detailed medical history, a strict physical examination had carried out, and confirmed to have different degrees of cerebral infarction, cerebral hemorrhage. The clinical degree of dementia (CDR) and the ability of daily living (ADL) test proved that there is dementia and decreased daily living ability. The neurological deficit score and cognitive function assessment were performed.

2 Methods of administration

Both groups were treated with oral enteric-coated aspirin 100 mg, 1 time/day, and nimodipine 30 mg/time, 3 times/day. The treatment group was additionally given the capsules of Cistanche glycoside, 2 capsules/time, 3 times/day, for 16 weeks. The control group was given Naofukang 800mg, 3 times a day for 16 weeks. During the experiment, no other drugs that improve cognitive function were taken.

Click to Cistanche effect for Domentia

1.3 Efficacy evaluation

MMSE is used to detect the cognitive function of the patient before medication and every 4 weeks after medication. CDR is used to detect the degree of dementia of the patients, and ADL is used to detect the self-care ability of the patient in daily life.

1.4 Evaluation of safety and tolerability

The evaluation of safety and tolerability is carried out every 4 weeks until the end of the 16th week. Including adverse reactions, corresponding physical examinations and neurological examinations, vital signs examinations (body temperature, blood pressure, pulse, and body weight), laboratory examinations (blood and urine routine, liver function, and blood biochemistry), electrocardiogram, before treatment, Compare later.

1.5 Statistical analysis

The Z test and Chi-square test were used before and after treatment, as well as the total Xihuanrong and the control group.

2. The results

2.1 MMSEXDR and ADL scores before treatment of boils are shown in Table 1.

Table 1: Comparison of the scoring results of the scales in the two groups before treatment (five s, points)

2.2 Comparison of the cognitive function (MMSE score) of the two groups

After treatment, the MMSE score of the Cistanche glycoside group was significantly different from that of the control group (P<0.01), as shown in Table 2. The difference between the self-control group after 16 weeks of treatment was statistically significant (P>0.01). See Table 3.

Table 2: Comparison of scale scores between the two groups at 16 weeks after treatment (Rex s, points)

Note: 2. Group MMSE, CDR, ADL comparison are all P<0.01

Table 3 The results of each scale before and after treatment in the meat hernia paste group (Yuanshi s, points)

2.3 The degree of dementia (CDR score)

After treatment, the CDR score of the Cistanche glycoside group was lower than that of the control group (P<0.05), as shown in Table 2. The self-control group was significantly lower after 16 weeks of treatment than before treatment (P>0 05). See Table 3.

2.4 The ability to support daily living (ADL score)

After treatment, the ADL score of the Cistanche glycoside group was lower than that of the control group (P>0.05), see Table 2; the self-control group was significantly lower after treatment than before treatment<P>0. 05). See Table 3.

2.5 Safety Before and after treatment

There were no obvious changes in blood routine and liver function and blood biochemistry. One case in the treatment group had diarrhea, and the relationship with the drug was uncertain.

3 Discussion

With the improvement of people's living standards, the incidence of vascular disease is also rising. There are two main problems affecting the life quality of patients with vascular diseases: neurological deficits and vascular dementia. Studies have shown that the incidence of vascular dementia after stroke is about 20%. Therefore, research on the mechanism of vascular dementia has also become an important topic. At present, the neurobiochemical, cellular, and molecular mechanisms that cause high-level intellectual damage after stroke have not yet been elucidated.

The main theories related to vascular dementia that currently exist are as follows:

(1) Cholinergic conduction pathways are damaged.

(2) Changes in the contact points and synapses between neurons. Synaptic damage is considered to be an early and common pathological change of neurological dysfunction diseases and is most closely related to cognitive impairment.

(3) Calmodulin (CaM), CaM-dependent protein kinase nCCaMPKH), as the most important molecules involved in memory in the hippocampus, are damaged during ischemia.

(4) Inflammation plays an important role in secondary neurological damage after acute cerebral ischemia

(5) Persistent oxygen free radical damage. Oxygen-free radicals play an important role in cerebral ischemia injury. The production and removal of oxygen free radicals in the normal body are in a dynamic balance. The defense system is damaged during cerebral ischemia, and the production of oxygen free radicals increases, attacking biological membranes, lipid peroxidation occurs, polyvalent unsaturated fatty acids are destroyed, and toxic intermediate products are generated ( Such as lipo oxygen peroxide), and the final product malondialdehyde. Malondialdehyde can cross-link the amino groups on proteins and phospholipids, reduce membrane fluidity, cause cell deformation, and impair function.

The cistanche glycoside is extracted from the cistanche tubulosa from northern Xinjiang. The main component is Cistanche phenylethanoid glycoside. Studies have found that cistanche glycoside is a strong antioxidant. The cistanche glycoside has been proven to have antioxidant effects, including anti-lipid peroxidation, scavenging superoxide anion, and inhibiting and scavenging hydroxyl free radicals. This article confirms that Cistanche glycoside can significantly improve the cognitive function of patients with vascular dementia, reduce the degree of dementia, and improve the ability of daily living. The possible mechanism is to protect brain tissue from ischemic damage by increasing the activity of brain tissue antioxidant enzymes and inhibiting lipid peroxidation. The specific mechanism of action still needs further clinical research.

references

[1J Pchjasvaare T, Erkinjuntti T, Ylinkoski R. Clinical determinate of post stroke denmentia[J]. Stroke, 1998, 29（1); 75.

[2] Li Wei, Jiang Ligang, Xu Zhongxin. Central nervous system apoptosis and delayed neuron necrosis in mice with experimental vascular dementia. Chinese Journal of Clinical Rehabilitation, 2005, 9 (28): 133-135.

[3] Jones CR, Hiley CR, Pelton JT, et al. Autoradiogra of the binding sites for[ 125IJ endothelin in rat and human brain[J]. Neurosci Lett, 1989,97(3):276- 279.

[4] Zhong Jianxin, Chen Keqiang, Lai Suipian, et al. Edaravone combined with low-molecular-weight heparin calcium in the treatment of progressive cerebral infarction [J]. Chinese Journal of Practical Nervous Diseases, 2007, 10 ⑶ M6-48.