The Killing Effect And Morphological Study Of Ultrasound And Hematoporphyrin Derivatives On EAT

At present, tumor has became one of the mainly vital diseases that are threatening people' s health. Apart form the surgical, actinotherapy and chemotherapy, many new treatments have been invented in latterly several decades such as High Intensity Focused Ultrasound surgery(HIFU), Ultrasound thermal treatment(UTT) and sonodynamic therapy(SDT). Compared with HIFU and UTT, SDT brought forward by Shin-ichiro V memura, a Japanese scholar, in 1989, has been a promising therapy for it' s being easier to focus, cheap equipments and avoiding thermal side-effect ,etc. The antitumor effect of SDT is based on the cooperated effects of ultrasound and photosensitive drugs(such as hematoporphyrin). In order to apply this method to clinic, domestic and overseas studies on the human cancer cells in vitro and animal tumors in vivo have accumulated some data and information for the mechanism and applications, but these are not sufficient for the complexity of the mechanism and the antitumor effects in vivo.This paper is a part work of "The cytological molecular biology mechanism of ultrasound activating HpD" , supported by National Nature Science Foundation. We applied 2.0MHz ultrasound and 2.5mg/ml Hematoporphyrin to observe the antitumor effects on Ehrlich ascites tumor(EAT)in vivo. The main conclusions as follow:1. The EAT cells absorbed HpD was observed through fluorescence-microscope, we ensured cancer cells could obtain the maximum HpD when they were treated through giving an appropriate time for absorbing.2. Three minutes was a sensitive treating time for EAT cells treated by SDT, the frequency of ultrasound was 2.0MHz and the power was 1.0W/cm2. The longer treating time could not give more serious injures and the EAT cells were treated 3 minutes had lingering damages.3.We clarified the degree and characteristics of injury of microstructure and ultramicrostructure of membrane system and inheritance information-expression system of EAT cells under different intensity of US. At the same time, we analysed sensitive sites of cell damage and preliminarily studied the effect of SDT.4. Through morphology study and fluorescent staining(PI-HCK AV-PI), we discovered the phenomenon which HpD activated by US could induce apoptosis of EAT cells firstly. We discussed the number and transforming of necrosis that was caused by direct damage and apoptosis at different intensity. We put forward that SDT induced apoptosis was an important way of antitumor.5. In damaged structure of EAT tumor in vivo, the injury of micro-blood vessel were visible through EM as well as LM. The damage of tumor tissue caused by SDT should be multiple and complex for the death of tumor cells can ensue these injury.6. Through the inhibition of tumor growth, twi-treatment with SDT can produce obviously inhibition effects which not only double the inhibition rate but also prolong the time of inhibition.