Effects of Panax notoginseng saponins on proliferation and apoptosis of vascular smooth muscle cells

Xu, Liang; Liu, Juntian; Liu, Na; Lu, Peipei; Pang, Xiaoming

doi:10.1016/j.jep.2011.05.020

Cited by 31 publications

(15 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In quiescent RASMCs that were induced by serum starvation for 24 h, the American ginseng extract did not exhibit any cytotoxic effects below the concentration of 200 μg/ml (data not shown). The observed cytotoxic effects of the American ginseng extract (>200 μg/ml) are consistent with the previous report that crude extract of Panax notoginseng (200, 400, 800 μg/ml) induced VSMC apoptosis (Xu et al, 2011). Thus, we used the American ginseng extract at a non-cytotoxic dose of 50 μg/ml to exclude any potential vascular toxicity of American ginseng in our study.…”

Section: Resultssupporting

confidence: 92%

“…In an effort to understand the putative beneficial effect of ginseng for the treatment of cardiovascular disease, it has been demonstrated that crude extracts of Panax ginseng or Panax notoginseng induce VSMC apoptosis and inhibit VSMC proliferation, thereby attenuating vascular lesion formation (Wu et al, 2001; Xu et al, 2011; Yu et al, 2011; Zhang et al, 2012). Increasing nitrogen monoxide (NO) formation or inactivating ERK is proposed to be critical for ginseng-induced growth inhibition in VSMCs, while up-regulating expression of p53, Bax, and caspase 3 is postulated to be crucial for ginseng-induced VSMC apoptosis.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

American ginseng inhibits vascular smooth muscle cell proliferation via suppressing Jak/Stat pathway

Wang

et al. 2012

Journal of Ethnopharmacology

View full text Add to dashboard Cite

Ethnopharmcological relevance Ginseng, a folk medicine which has been used for thousands of years in Asia, has been promoted for the treatment or prevention of health problems including cardiovascular disease. However, the molecular mechanism of ginseng-induced cardiovascular protection is unclear. Thus, we investigated signaling mechanism by which American ginseng inhibits vascular smooth muscle cell (VSMC) proliferation, a key feature of diverse vascular disease. Materials and methods A standardized crude extract of American ginseng was supplied by the National Research Council of Canada, Institute for National Measurement Standards. Rat aortic smooth muscle cells (RASMCs) were exposed to fetal bovine serum (FBS), platelet derived growth factor (PDGF), insulin, or angiotensin II (Ang II) to induce proliferation that was examined by measuring DNA synthesis and cell numbers. Western blot was applied to determine the activations of Jak, Stat, Akt, and ERK. Results American ginseng inhibited RASMC proliferation induced by FBS, PDGF, insulin or Ang II. American ginseng slightly increased both basal and FBS-, PDGF- or Ang II-induced activities of Akt and ERK in RASMCs; however, it dramatically inhibited the activation of Jak2 and Stat3. Conclusion These results demonstrate that American ginseng inhibits VSMC proliferation through suppressing the Jak/Stat pathway.

show abstract

Section: Resultssupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

American ginseng inhibits vascular smooth muscle cell proliferation via suppressing Jak/Stat pathway

Wang

et al. 2012

Journal of Ethnopharmacology

View full text Add to dashboard Cite

show abstract

“…Moreover, the quantitative analysis revealed that PNS treatment was associated with a reduction in intralesional SMCs, particularly in the high-dose PNS-treated mice. In this regard however, the effect of PNS on foam cells and SMCs might have contributed to its effect on plaque reduction [11,19]. Interestingly, PNS treatment in the present study was found to enhance lesion endothelialization and rapid reendothelialization, which may effectively attenuate the aggregation of foam cells, proliferation of SMCs, and limit the extent of atherosclerotic plaque formation after vascular injury [20,21].…”

Section: Discussionmentioning

confidence: 83%

Panax NotoginsengSaponins Promote Endothelial Progenitor Cell Mobilization and Attenuate Atherosclerotic Lesions in Apolipoprotein E Knockout Mice

Liu

Fei

Zhang

et al. 2013

Cell Physiol Biochem

View full text Add to dashboard Cite

Background: Endothelial progenitor cells (EPCs) derived from the bone marrow (BM) play a key role in the homeostasis of vascular repair by enhanced reendothelialization. Panax notoginseng saponins (PNS), a highly valued traditional Chinese medicine, has been shown to reduce morbidity and mortality from coronary artery disease. The present research was designed to explore the contribution of progenitor cells to the progression of atherosclerotic plaques and the possible modulatory role of PNS in this process. Methods: PNS (60 or 120 mg/kg via intraperitoneal injection) was administered over 8 weeks in apolipoprotein E knockout mice on an atherogenic diet. The sizes and histochemical alteration of atherosclerotic lesions and numbers of EPCs in BM and peripheral blood were analyzed. The expression of chemokine stromal cell-derived factor 1α (SDF-1α) and its receptor, CXCR4, was monitored as well. Results: PNS significantly reduced the lesion area and intima-to-media ratio compared to vehicle treatment. PNS also augmented endothelialization and reduced the smooth muscle cell (SMCs) content of the lesions. The number of c-kit and sca-1 double-positive progenitor cells and flk-1 and sca-1 double-positive progenitor cells were significantly increased in the BM and the peripheral blood of the PNS-treated groups. PNS treatment increased the plasma levels of SDF-1α and SCF as well as the BM levels of matrix metalloproteinase-9 (MMP-9). Moreover, the mRNA levels of SDF-1α and protein levels of CXCR4 were both increased in the BM of mice treated with PNS, while SDF-1α expression decreased. Conclusion: PNS reduce the size of atherosclerotic plaques, and this effect appears to involve progenitor cell mobilization. SDF-1α-CXCR4 interactions and the possible modulatory role of PNS in this process may contribute to the increased progenitor cell mobilization.

show abstract

“…The ratio of bax/bcl‐2 is very crucial for the determination of cell survival and death (Xu, Liu, Liu, Lu, & Pang, 2011). Curcumin‐induced apoptosis particularly involves the mitochondria‐mediated pathway in different cancer cells.…”

Section: Discussionmentioning

confidence: 99%

A study on effect of curcumin on anticerebral aneurysm in the male albino rats

Miao

Wang

et al. 2017

Brain and Behavior

View full text Add to dashboard Cite

IntroductionThis study investigated the curcumin effect on the cerebral aneurysm. Apoptosis is known to play a fundamental role in the pathogenesis of a cerebral aneurysm. Therefore, we investigated the effect of curcumin on apoptosis of smooth muscle cells of a cerebral aneurysm‐induced male albino rats.MethodsIn this study, the cerebral aneurysm has been induced in the male albino rats by the CaCl2 administration. After cerebral aneurysm induction, smooth muscle cells were isolated. Cells were treated with curcumin (25 & 50 mg/kg bwt) for 48 hr.ResultsCurcumin reduced altered mitochondrial morphology significantly, evidenced through fluorescence and confocal study. Curcumin treatment reduced the expression of p53, caspase‐3, and bax/bxl‐2 ratio significantly. Curcumin treatment also reversed the cellular architecture of smooth muscle cell wall significantly. Fluorescence and the confocal study confirmed the reduction in apoptosis in a cerebral aneurysm‐induced smooth muscle cells of male albino rats.ConclusionTaking all these data together, it may suggest that the curcumin could significantly reduce the CaCl2‐induced cerebral aneurysm through the inhibition of cell apoptosis in the cells.

show abstract

Effects of Panax notoginseng saponins on proliferation and apoptosis of vascular smooth muscle cells

Cited by 31 publications

References 22 publications

American ginseng inhibits vascular smooth muscle cell proliferation via suppressing Jak/Stat pathway

American ginseng inhibits vascular smooth muscle cell proliferation via suppressing Jak/Stat pathway

Panax NotoginsengSaponins Promote Endothelial Progenitor Cell Mobilization and Attenuate Atherosclerotic Lesions in Apolipoprotein E Knockout Mice

A study on effect of curcumin on anticerebral aneurysm in the male albino rats

Contact Info

Product

Resources

About