Applications of Notoginseng triterpenes

Notoginseng triterpenes（Ginsenoside Mb; Ginsenoside C-Mc1; NOTOGINSENOSIDE-FE; Notoginsenoside-Fe, 98%; notoginseng triterpenes; panax notoginseng leaves; Notoginseng leaf saponins; Radix Notoginseng Extract;Notoginseng total saponins; total saponins of Notoginseng; C47H80O17）[2] is a natural compoud isolated from Panax japlcus var[3].

Notoginseng triterpenes have been used for the treatment of coronary heart disease, heart failure and other cardiovascular diseases. Notoginseng triterpenes can promote EA-hy926 cell proliferation, angiogenesis and expression of VEGF protein[4].
Panax notoginseng saponins(PNS) is an effective traditional medicine for the treatment of atherosclerosis(AS). It can effectively prevent and treat AS induced by inflammatory reactions as a result of its anti-inflammatory effects, its ability to decrease blood lipid levels and its ability to regulate vessel function. One of the main mechanisms by which PNS exerts its anti-inflammatory effects is by inhibiting the translocation of p65 NF-κB into the nucleus, which results from the induction of IκB expression and inhibition of NF-κB expression. PNS regulates blood vessel activity by regulating the expression of the Anf, Edn and F3 genes[5]. 

Ginsenoside Rg1 is one of the main compounds responsible for the pharmaceutical actions of PNS. In a study that after induction of vascular injury and thrombosis by 10% FeCl on mesenteric arterioles of wild-type B57/b6 mice, the injection of ginsenoside Rgl can significantly reduce platelet adhesion and thrombosis, prolong vascular occlusion time[6].

Zhang et al. also found that ginsenoside Rg1 exerted a neuroprotective role on the oxygen/glucose-deprived hippocampal neurons and slices, as well as on the ischemic/reperfused brain in rats. This effect is probably mediated by the activation of glucocorticoid receptors, the inhibition of Ca2+ influx through both NMDA receptor channels and L-type voltage-dependent Ca2+ channels, and the resultant reduction of intracellular free Ca2+. As a result, neuronal death including apoptotic cell death is diminished[7].

Besides, Kumitko Kitamura et al. discovered that Panax notoginseng roots increase glucose uptake in muscles using an in vitro screening test (unpublished data). Dammarane-type triterpene extract (DTE) from Panax notoginseng roots had stronger suppressive activity on blood glucose levels and improved oral glucose tolerance, insulin sensitivity, glucose uptake, and Akt phosphorylation in skeletal muscle, which suggested that DTE can be a promising agent for controlling hyperglycemia by enhancing glucose uptake in skeletal muscle[8] .
Also, notoginseng triterpenes can alleviate the elderly anxiety disorder[9].
 

References

[1]https://www.google.com.hk/search?q=Notoginseng+triterpenes&safe=strict&hl=zh-CN&tbm=isch&source=iu&ictx=1&fir=GkWG28VdWhoC2M%253A%252C7wlSXSCFKlq2iM%252C_&vet=1&usg=AI4_-kQihOhhD_wlB_F5f8WfEmrruCzQlw&sa=X&ved=2ahUKEwj-x9qLlPfkAhXBMd4KHVm_CYMQ9QEwB3oECAkQBg#imgrc=s366T-byRB2q3M:&spf=1569798911807&vet=1
[2]https://www.chemicalbook.com/ChemicalProductProperty_EN_CB7855223.htm
[3]https://www.medchemexpress.com/Notoginsenoside-Fe.html
[4]Shi HB, Chen JD, Chen XH, He Y, Yang ZJ. Effects of salvianolic acid and notoginseng triterpenes on angiogenesis in EA-hy926 cells in vitro[J]. Chinese Journal of Natural Medicines 2013, 11(3): 254-257.
[5]Zhang YG, Zhang HG, Zhang GY, et a1. Panax notoginseng saponins attenuate atherosclerosis in rats by regulating the blood lipid profile and an anti-inflammatory action[J].Clinical and Experimental Pharmacology and Physiology, 2008, 35(10): 1238-1244.
[6]Zhou Q, Jiang L, Xu C, et a1. Ginsenoside Rgl inhibits platelet activation and arterial thrombosis[J]. Thrombosis Research, 2014, 133(1): 57-65.
[7]Zhang YF, Fan XJ, Peng LL, et a1. Ginsenoside Rgl protects neurons from hypoxic-ischemic injury possibly by inhibiting Ca2+ influx throurgh NMDA receptors and L-type voltage-dependent Ca2+ channels[J]．European Journal of Pharmacology, 2008, 586(1-3): 90-99．

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