| Ligusticum chuanxiong Hort. is one of famous traditional Chinese drugs for curing many illnesses. Chemical components of chuanxiong are complicated, including phthalide, phenolic acid, coriander and so on. Tetramethylpyrazine and ferulie acid are the most important officinal ingredient. Many researches have revealed that FA possesses plenty of beneficial pharmacological effects such as inhibiting macrophages activation and platelets activation and improving endothelial function, improving microcirculation relieving oxidative stress, which can be used for many clinic illnessxardio-cerebrovascular disease, haematological diseases, urinary injury, respiratory system diseases and so on. The planting has become larger, however, it was short because of the destruction of natural environment, unlimited exploiting and cult technology, it cannot settle for the demand. Utilizing cell engineering to solve the matter is another approach.This study included two aspects:1,The culture condition of tissue and the analysis of karyotype:Fresh shoots of Ligusticum chuanxiong Hort. were used as explants in the culture tissue. It was callus cultivation system, the influent of grow times on secondaty metabolism, the karyotype of callus in this experiment. It is discovered that the addition of 2,4-D(2.0mg/L) and 6-BA(0.4mg/L) in MS culture metrix is suitable to induce callus. The suitable for further grow is 2,4-D (0.5mg/L) in MS culture metrix. The karyotype formula is K(2n)=11X=22=16m+4sm+2st(SAT), among them 8 pairs are metacentric(m), 2 pairs are submetacentric(sm) and 1 pair is acrocentric chromosome(st).The content of secondary metabolism was increase with the incubation time.2,How to protect brain by Ferulic acid and the mechanism:On the basis of establishment of two brain-trauma model of rats: the brain injury model and AD model which induced by using aggressive Aβ1-40 and KA in rat hippocampus. We firstly observe the protective effect of FA on experimental brain-trauma rats, then investigate its relative mechanism at different level using different methods. We believe this work would be helpful to provide some valuable evidence for application of FA against brain injury.①To evulate effects of FA on experimental brain injury model of mice by brain trauma and investigate the mechanism:Sixty mice were divided into five groups: the normal group, the brain injury model groups, the high dose group, the middle dose group and the low dose group, each 10. Refering to the Free-Falling-Body-Crash-Divice of Feeney and traumatic with open, the brain-injury model was established. The mice were administrated with FA three days later, then once a day. The normal mice and model mice were given the same quantity of normal saline for 7d. The mice were killed by pulling neck. The brains were immediately removed. Measurement of brain water contents after traumatic brain injury.After wet weighted, the mass of tissue was then settled in a roasting cheset(100℃)and being baked for 24 hours, and its dry weight was measured. Water content was calculated by (wet weight-dry weight)/wet weight. One brain slice beyond the injured field, were made into frozen sections, and sent to HE and Nissle stain. One brain slice was stored in a refrigeratory to investigate the brain NO and the mitochondria ATP after traumatic brain injury. Results: Observed by light microscope, in the normal group, brain cells were arrayed in an orderly manner with regular nucleus, obvious nucleolus, more cytoplasm without cerebral edema. The neurons in brain were impaired, the difference between nucleolus and cytoplasm were not clearly, nucleolus disappeared, some holes in the tissue. After treated with FA, the degree of damage were alleviated by contrast to the model group. The content of NO was increased in the mouse with brain trauma, the activity of the mitochondria ATPase was significant decreased in the mice with brain trauma. After treatment, this phenomena grown better.Conclusions: The brain-trauma mouse model could be established by the Free-Falling-Body-Crash-Divice of Feeney; Treatment with FA can reduce brain edema, reduce the content of NO and improve the activity of mitochondria ATPase after the brain trauma in the mice. Therefore the secondary damage to the brain can be relieved and the prognosis of the brain trauma can be improved.②To evulate effects of FA on experimental brain injury model of rat by using aggressive Aβ1-40 and KA in rat hippocampus and investigate the mechanism:Thirty SD rats were divided into five groups:the normal group, the AD model groups, the high dose group, the middle dose group and the low dose group, each 6. We used the animal model of AD by stereotaxic damage of rat hippocampus using aggressive Aβ1-40 and KA in this experiment. And the rats were given saline v/hich was injected into the same field, in order to replace Aβ1-40 and KA as the normal group. After the model established, the treatment groups were given FA(different concentration), while the normal rats and model rats were given the same quantity of normal saline, uninterrupted treat for 20 d. Three hours later, after the last treatment, rats were sacrificed by decapitation.The brains were immediately removed.They were washed with cold normal saline thoroughly, and then suck up unnecessary moisture with filter paper. Then the brain were used to determine the biochemistry data of SOD, GSH-PX and MDA.ResuIts: Quantiative analysis indicated that the SOD and GSH-PX activities decreased and the MDA level increased in the senile model group, compared with the normal group. In contrast with those in the SOD,GSH-PX activities increased and the MDA level decreased in the medicine groups.Conclusions: FA, as a antioxidant, exerted antioxidant action by scavenging free radical, enhancing the activities of SOD and GSH-PX, and decreasing the contents of MDA in the Aβ1-40 and KA induced AD model group; FA can provide protection for oxidant damage of alzheimer's disease model rats in a certain extent, which may be used for AD.
|
PDF Full Text Request