觀察赤土茯苓苷(Smi)對動物實驗性胃潰瘍的作用。以昆明種小鼠和Wistar大鼠為實驗材料,通過3種胃潰瘍動物模型判斷藥效。結(jié)果:Smi對小鼠利血平型、應(yīng)激型及大鼠幽門結(jié)扎型胃潰瘍均有保護作用。Smi各組:潰瘍指數(shù)、出血點數(shù)均明顯小于生理鹽水組(Smi100、200mg/kgP<0.05;Smi300mg/kg P<0.01);提高應(yīng)激型小鼠胃粘膜Se-GSH-Px活力(P<0.05),降低MDA含量(Smi100、200mg/kg P<0.05,Smi300mg/kg P<0.01);提高幽門結(jié)扎型大鼠胃液量、胃液 pH(Smi10 0、200mg/kg P<0.05,Smi300mg/kg P<0.01)。各組均對胃蛋白酶無顯著影響(P>0.05);對小鼠胃腸推進蠕動無影響(P>0.05)。結(jié)論:Smi有明顯的防治胃潰瘍的作用。這可能與其增加胃粘膜 Se- GSH- Px活力、降低MDA含量,減輕自由基對胃粘膜的損害有關(guān)。

Protective effects of smiglabran (SM),a glucoside isolated from Smilax glabra Roxb.,on experimental models of peptic ulcersinduced by reserpine,stress and pylorus ligation were studied.SM at doses of 100 ～ 300 mg /kg resulted in a decrease of peptic ulceration index and number of blood clots,increased the Se-GSH-Px activity of gastric mucosa,lower the amount of malondialdehyde (MDA) and elevated gastric fluid and pH levels as compared with the normal saline control,but without effects on pepsin and gastrointestinal peristalsis.These results indicated that SM could obviously prevent pepticulceration probably through its actions to enhance Se-GSH-Px activity and lower MDA and free radical damage on gastric mucosa.