<i>Panax notoginseng</i> Promotes Repair of Colonic Microvascular Injury in Sprague‐Dawley Rats with Experimental Colitis

Wang, Shiying; Peng, Tao; Zhao, Lei; Zhang, Wangjun; Hu, Hong-Yi; Lin, Jianghai

doi:10.1155/2018/4386571

Cited by 6 publications

(11 citation statements)

References 23 publications

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“…P N h a s b e e n s h o w n t o p r o m o t e a n g i o g e n e s i s , regulate metabolism, and reduce the inflammatory response (17). Our previous research also found that PN could significantly promote angiogenesis and reduce vascular inflammatory injuries in colitis (3,4). Indeed, some saponins in PN, which are important active chemical components including ginsenosides and notoginsenosides, have appeared to lack toxicity in both animals and humans (5).…”

Section: Discussionmentioning

confidence: 89%

“…TSP1 is a critical protein involved in increasing vascular injuries and promoting vascular remodeling (13,14). Our results in previous studies showed that PN could significantly regulate the secretion of VEGFA165 and VEGFA121 and down-regulate the expression of TSP1 protein in colonic mucosa (3). However, the regulatory effect of NGR2 on the Rap1GAP/PI3K/ Akt signaling pathway is unclear.…”

Section: Introductionmentioning

confidence: 85%

“…Histopathology, MVD, cell viability assay, cell proliferation assay, tube formation assay, plasmid construction and cell transfection, and western blotting were carried out as previously described (12). The VP and MP in the colon were detected as previously described (3,15). All assays were performed at least 3 times.…”

Section: Histopathology Microvessel Density (Mvd) Vascular Permeability (Vp) Mucosal Permeability (Mp) Cell Viability Assay Cell Prolifermentioning

confidence: 99%

“…The formation of granulation tissue during the repair of traumatic injuries is the result of the controllable regulation of angiogenesis, including promoting angiogenesis and anti-angiogenesis (1), which have been shown to be regulated by PN (2). Our previous research found that PN could significantly promote angiogenesis and reduce vascular inflammatory injuries (3,4). Indeed, some saponins in PN, which are important active chemical components including ginsenosides and notoginsenosides, have appeared to lack toxicity in both animals and humans (5).…”

Section: Introductionmentioning

confidence: 99%

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Notoginsenoside R2 induces colonic microvascular injuries via regulating the Rap1GAP/PI3K/Akt signaling pathway

Peng¹,

Lin²,

Zhang³

et al. 2021

Ann Transl Med

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Background: Notoginsenoside R2 (NGR2) is an important active saponin molecule of Panax Notoginseng (PN), but its effect on regulating angiogenesis is unclear. Here, we investigated the role of NGR2 in angiogenesis in vivo and in vitro.Methods: NGR2 was administered to rats by intragastric administration for 7 days. The colonic histopathology and microvessel density (MVD) were observed and evaluated under an inverted microscope.The colonic mucosal permeability (MP) and vascular permeability (VP) were evaluated by measuring the transmittance of FD-4 and the vascular leakage of Evans blue, respectively. The serum IL-2, TNF-ɑ, IL-4, IL-10, VEGFA165, and VEGFA121 levels were detected with ELISA. In vitro, pHUVECs were cultured and treated with NGR2. The mechanism of NGR2 in angiogenesis was assessed by VEGFA165, LY294002, silencing, and overexpression plasmids of Rap1GAP in vitro. The cell viability, cell proliferation, tube formation, and concentration of intracellular pyruvate and lactic acid of pHUVECs were measured after 24 h. The expression of proteins was detected with western blotting.Results: NGR2 could significantly induce inflammatory injuries in the colonic mucosa and microvessels.Both MP and VP in rats treated with NGR2 increased in proportion to the serum VEGFA165 and VEGFA121 level, the ratio of VEGFA165/VEGFA121, and the concentration of intracellular pyruvate and lactic acid. In vitro, NGR2 reduced cell viability, proliferation, and tube formation, and enhanced the intracellular glycolysis of pHUVECs. Furthermore, the cell viability, proliferation, and tube formation of pHUVECs were inhibited by NGR2 via blocking the Rap1GAP/PI3K/Akt signaling pathway.Conclusions: NGR2 could induce colonic mucosal microvascular injuries and promoted the intracellular glycolysis of pHUVECs via blocking the Rap1GAP/PI3K/Akt signaling pathway.

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Section: Discussionmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 85%

Section: Histopathology Microvessel Density (Mvd) Vascular Permeability (Vp) Mucosal Permeability (Mp) Cell Viability Assay Cell Prolifermentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Notoginsenoside R2 induces colonic microvascular injuries via regulating the Rap1GAP/PI3K/Akt signaling pathway

Peng¹,

Lin²,

Zhang³

et al. 2021

Ann Transl Med

Self Cite

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“…Ginsenosides Rb1 and Rg1 activate and produce NO by regulating the PI3K/Akt/eNOS signal pathways and arginine transformation on endothelial cells, so as to increase the endothelium-dependent hemangiectasis in rats (Pan et al, 2012 ). Our recent study found that Panax notoginseng could promote repair of injuries of colonic mucosa and microvessels via downregulating VEGFA isoforms and inhibiting Rap1GAP/TSP1 signaling pathway (Wang et al, 2018 ). Gallic acid (Chang et al, 2015 ), a primary active ingredient of Galla chinensis, has multiple bioactivities like anti-inflammation, anti-mutation, anti-oxidation, and anti-free radicals.…”

Section: Discussionmentioning

confidence: 99%

Qingchang Suppository Ameliorates Colonic Vascular Permeability in Dextran-Sulfate-Sodium-Induced Colitis

et al. 2018

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Ulcerative colitis (UC), with a long course and repeated attack, severely affects patient's life quality and increases economic burden all over the world. However, the concrete causes and mechanisms of UC are still unclear, but it is generally considered that many factors participate in this process. Qingchang Suppository (QCS) has been used in treating rectitis and colitis for about 30 years in Shanghai, China. Its satisfactory clinical effects have been proved. The aim of this study is to investigate the effect and mechanisms of QCS on colonic vascular endothelial barrier in dextran sulfate sodium (DSS)-induced colitis. The results indicated that increased vascular permeability (VP) appeared earlier than increased intestinal epithelial permeability (EP) in the process of DSS-induced colitis. QCS attenuated colonic tissue edema, vascular congestion and inflammatory cell infiltration. QCS inhibited the elevation of MPO, TNF-α, and IL-6 levels in colon tissues and alleviated the microvascular damage induced by DSS. QCS also improved colonic hypoxia and decreased the expression of VEGF, HIF-1α, and iNOS. These results revealed that QCS can reduce colonic VP and can improve vascular endothelial barrier function maybe by regulating the VEGF/HIF-1α signaling pathway.

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Medicinal herbs and teas

Vezza¹,

Ruiz-Malagón²,

Rodríguez-Sojo³

et al. 2023

Natural Plant Products in Inflammatory Bowel Diseases

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Panax notoginseng Promotes Repair of Colonic Microvascular Injury in Sprague‐Dawley Rats with Experimental Colitis

Cited by 6 publications

References 23 publications

Notoginsenoside R2 induces colonic microvascular injuries via regulating the Rap1GAP/PI3K/Akt signaling pathway

Notoginsenoside R2 induces colonic microvascular injuries via regulating the Rap1GAP/PI3K/Akt signaling pathway

Qingchang Suppository Ameliorates Colonic Vascular Permeability in Dextran-Sulfate-Sodium-Induced Colitis

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