Panax notoginseng Saponins Attenuate Atherogenesis Accelerated by Zymosan in Rabbits

Liu, Ya; Zhang, Haigang; Jia, Yong; Li, Xiaohui

doi:10.1248/bpb.33.1324

Cited by 45 publications

(27 citation statements)

References 57 publications

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“…In accordance with our previous findings in rabbit and rat experiments [9,18], satisfactory anti-atherogenic effect of PNS on apoE -/- mice was observed, displaying decreased size of aortic plaques, reduced ratio of intima-to-media, and alleviation of atherosclerotic pathological changes in arteries. Moreover, the quantitative analysis revealed that PNS treatment was associated with a reduction in intralesional SMCs, particularly in the high-dose PNS-treated mice.…”

Section: Discussionsupporting

confidence: 92%

“…Various reagents of PNS, such as Panax notoginseng saponins Injection (Xue Sai Tong Injection), freeze-drying powder of Panax Notoginseng Saponins for Injection are applied clinically in China and are well established to reduce morbidity and mortality from coronary artery disease [7,8], meeting the criterion of the Pharmcopoeia of the People's Republic of China 2010. In addition to the lipid-lowering effects associated with PNS, our previous studies on the anti-atherogenic effects of PNS have shown that it is capable of reducing vascular inflammation, modulating endothelial dysfunction, and decreasing the formation of foam cells via pleiotropic mechanisms [9,10,11,12]. However, the potential role of PNS on EPCs during atherogenesis has not been systematically evaluated.…”

Section: Introductionmentioning

confidence: 99%

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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

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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.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

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

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“…In our previous studies we have addressed the role of PNS in the progression of atherosclerosis and to explore the possible relevant molecular mechanisms. The results showed that PNS treatment significantly decreased the mRNA expression levels of MCP-1 and NF-κB/p65 in the aorta wall after 8 weeks of treatment, indicating that PNS attenuates atherogenesis through an anti-inflammatory action [23]. In addition, the observations in lipopolysaccharide (LPS)-stimulated mouse macrophage cells, RAW264.7 cells suggested that PNS have a strong anti-inflammatory property to suppress the expression of the inflammation-associated genes including inducible nitric oxide synthase, cycloxygenase-2, tumor necrosis factor-alpha and interleukin-1beta by inhibiting the NF-κB activation, resulting in its anti-inflammatory effects [24].…”

Section: Discussionmentioning

confidence: 92%

Panax Notogingseng Saponins Suppress RAGE/ MAPK Signaling and NF-kappaB Activation in Apolipoprotein-E-deficient Atherosclerosis-prone mice

Dou

Lu²,

Shen³

et al. 2012

Cell Physiol Biochem

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Background: Panax notoginseng saponins (PNS) extracted from the roots of panax notoginseng are free radical-scavenger, with an antioxidant property, capable of inhibiting expression of adhesion molecules and chemokines. This study was designed to test the effects of PNS administration in apolipoprotein (apo)-E-deficient mice on the activation of JNK, p38^MAPK, ERK1/2 and NF-ĸB, and the expression of RAGE, adhesion molecules and chemokines in the atherosclerotic lesions. Methods: Wild type and apoE-null mice (male, 10-week-old) were treated with PNS for 4 weeks. Peripheral blood was collected for assessing the serum levels of glucose, lipids and MDA, and activities of SOD and GSH. The sizes of atherosclerotic lesions and numbers of macrophages in the branchiocephalic arteries, and the reactive oxygen species (ROS) production in the aortic root were analyzed. The levels of CD68, Galectin-3, RAGE, JNK, phosphor-JNK, p38^MAPK, phosphor-p38^MAPK, ERK1/2, phosphor-ERK1/2, I-ĸB, phosphor-I-ĸB (Ser32), NF-ĸB, phosphor-NF-ĸB, MCP-1, VCAM-1 and ICAM-1 in the descending arteries were identified by Western blot. Results: The atherosclerotic lesion sizes, and macrophage numbers, but not the smooth muscle cell amounts and the collagen content, were decreased in apoE^-/mice treated with PNS. After PNS administration for 4 weeks, the apoE^-/-mice displayed reduced level of serum MDA and enhanced activity of SOD and GSH, accompanied by impaired ROS generation in the aortic root. Moreover, PNS down-regulated the expression of VCAM-1, ICAM-1 and MCP-1, accompanied by reduced expression of RAGE and suppressed the activation of NF-ĸB, JNK, p38^MAPK and ERK1/2. Conclusion: PNS may inhibit progression of atherosclerotic lesions via their antioxidant/anti-inflammatory biological properties. PNS suppress the RAGE/MAPK signaling pathways, inactivate NF-ĸB, and reduce expression of pro-inflammatory factors, such as VCAM-1, ICAM-1 and MCP-1 in atherosclerotic lesions of apoE^-/-mice.

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“…Rats in groups III-VI were given intragastric ethanol infusions to induce chronic liver injury. The ethanol dose was increased gradually by using a method of Zhang 15) as follows: 5.0 g/kg/d from 1 to 4 weeks, 7.0 g/kg/d from 5 to 8 weeks, 9.0 g/kg/d from 9 to 12 weeks. Group III served as the ethanol-induced liver injury model.…”

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confidence: 99%

Retraction: Asiatic Acid from <i>Potentilla chinensis</i> Attenuate Ethanol-Induced Hepatic Injury <i>via</i> Suppression of Oxidative Stress and Kupffer Cell Activation

Wei

Huang

et al. 2013

Biological & Pharmaceutical Bulletin

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This study examined the effect of Asiatic acid from Potentilla chinensis (AAPC) on chronic ethanolinduced hepatic injury. Rats underwent intragastric administration of ethanol (5.0-9.0 g/kg) once a day for 12 weeks. A subset of rats were also intragastrically treated with AAPC (2, 4 or 8 mg/kg) once a day. In the end, AAPC treatment significantly protected against ethanol-induced liver injury, as evidenced by the decrease in serum alanine and aspartate aminotransferases levels and the attenuation of histopathological changes in rats. Additionally, AAPC significantly decreased blood alcohol and acetaldehyde concentrations by enhancing alcohol dehydrogenase and aldehyde dehydrogenase activities. Mechanistically, studies showed that AAPC remarkably alleviated the formations of malondialdehyde and myeloperoxidase, restored impaired antioxidants, including superoxide dismutase, glutathione peroxidase, glutathione reductase and catalase, and inhibited cytochrome P450 (CYP)2E1 activity. Moreover, the over-expression of cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), the elevated plasma endotoxin level and the up-regulated Toll-like receptor 4 (TLR4), CD14 and myeloid differentiation factor 88 (MyD88) as well as nuclear factor-κB were also suppressed by AAPC in ethanol-intoxicated rats. In conclusion, the protective effect of AAPC on ethanol-induced hepatotoxicity was mainly due to its ability to attenuate oxidative stress and inhibit Kupffer cell activation by decreasing the level of plasma endotoxin and the expression of TLR4, CD14 and MyD88.

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Panax notoginseng Saponins Attenuate Atherogenesis Accelerated by Zymosan in Rabbits

Cited by 45 publications

References 57 publications

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

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

Panax Notogingseng Saponins Suppress RAGE/ MAPK Signaling and NF-kappaB Activation in Apolipoprotein-E-deficient Atherosclerosis-prone mice

Retraction: Asiatic Acid from <i>Potentilla chinensis</i> Attenuate Ethanol-Induced Hepatic Injury <i>via</i> Suppression of Oxidative Stress and Kupffer Cell Activation

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