茉莉酸甲酯和水杨酸对西洋参愈伤组织生长和皂苷形成的影响

Effects of methyl jasmonate and salicylic acid on callus growth and saponins production of American ginseng

本文旨在探究不同诱导子对西洋参愈伤组织生长、相关酶活性及其人参皂苷含量的影响,在西洋参愈伤组织中,应用HPLC检测了添加诱导子茉莉酸甲酯(methyl jasmonate,MeJA)和水杨酸(salicylic acid,SA)后西洋参愈伤组织皂苷生物合成的变化。结果显示,MeJA抑制生长,但SA对其生长影响较小;2种诱导子均可以显著激活西洋参愈伤组织中超氧化物歧化酶(superoxide dismutase,SOD)、过氧化氢酶(catalase,CAT)、过氧化物酶(peroxidase,POD)活性和丙二醛(malondialdehyde,MDA)含量;培养基中MeJA浓度为100μmol/L时,愈伤组织中总皂苷含量和产量均达到最大值,人参皂苷Rg_(1)、Re、Rb_(1)、Rc的含量最高,在SA诱导子试验组中,当SA浓度为300μmol/L时,西洋参愈伤组织中总皂苷含量和产量均达到最大值,人参皂苷Rb_(1)的含量最高。结果表明,在西洋参愈伤组织中添加适当浓度MeJA和SA诱导子会提高人参皂苷化合物含量,其中以MeJA诱导人参总皂苷的效果最好,同时也会影响西洋参愈伤组织的生长量。说明在培养过程中添加外源诱导子,有利于提高西洋参愈伤组织中皂苷含量。

The aim of this study was to investigate the effects of different inducers on callus growth,related enzyme activities and ginsenoside content of American ginseng(Panax quinquefolium L.,AG).The changes of methyl jasmonate(MeJA)and salicylic acid(SA)on saponin biosynthesis in callus of AG were determined by HPLC.The results showed that MeJA inhibited the growth,but SA had little effect on the growth.Both inducers could significantly activate the activities of antioxidant enzymes superoxide dismutase(SOD),catalase(CAT),peroxidase(POD)and malondialdehyde(MDA)content in callus of AG.When the concentration of MeJA in the medium was 100μmol/L,the content and yield of total saponins in callus re-ached the maximum,and the contents of ginsenosides Rg _(1),Re,Rb_(1) and Rc were the highest.In the SA-induced sub-experimental group,when the concentration of SA was 300μmol/L,The content and yield of total saponins in callus of AG reached the maximum,and the content of ginsenoside Rb_(1) was the highest.The results showed that adding appropriate concentrations of MeJA and SA inducers in the callus of AG could increase the content of ginsenosides,and MeJA had the best effect in inducing total ginsenosides,and also affected the growth of AG callus.The results indicated that the addition of exogenous inducers was beneficial to increase the content of saponin in callus of AG.