A Korean herbal medicine, Panax notoginseng, prevents liver fibrosis and hepatic microvascular dysfunction in rats

Park, Won‐Hwan; Lee, Soo-Kyung; Kim, Cheorl-Ho

doi:10.1016/j.lfs.2004.07.030

Cited by 60 publications

(45 citation statements)

References 42 publications

(46 reference statements)

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“…Oxidative stress represents a direct or indirect pro-fibrogenic stimulus for HSC activation [28][29][30] . In the search for therapeutic strategies for hepatic fibrosis, many antioxidants show promising results [24,[30][31][32][33][34][35][36] , including ginseng extracts [22,37] . However, there are few reports that have evaluated the effects of Rg1 on hepatic fibrosis by inhibiting oxidative stress [21] .…”

Section: Discussionmentioning

confidence: 99%

“…Ginseng extracts have been reported to exert protective effects, in in vitro studies as well as in various animal and clinical models, in models of liver injury induced by a variety of hepatotoxins, including CCl 4 and alcohol [17,19,22,37,46] . However, research on the effect of Rg1 on liver fibrosis is limited [21] .…”

Section: Discussionmentioning

confidence: 99%

“…The molecular constituents responsible for the action of ginseng are ginsenosides, among which, Rg1 is the most abundant and active ingredient of P ginseng [14,16] . Several studies have shown that Rg1 or ginseng extract has a liver protective effect [16][17][18][19][20][21][22] . These findings strongly indicated that Rg1 is a potent antifibrotic agent.…”

Section: Introductionmentioning

confidence: 99%

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Nrf2 pathway activation contributes to anti-fibrosis effects of ginsenoside Rg1 in a rat model of alcohol- and CCl4-induced hepatic fibrosis

Gao

Chu

et al. 2014

Acta Pharmacol Sin

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Aim: To investigate the anti-fibrosis effects of ginsenoside Rg1 on alcohol-and CCl 4 -induced hepatic fibrosis in rats and to explore the mechanisms of the effects. Methods: Rats were given 6% alcohol in water and injected with CCl 4 (2 mL/kg, sc) twice a week for 8 weeks. Rg1 (10, 20 and 40 mg/kg per day, po) was administered in the last 2 weeks. Hepatic fibrosis was determined by measuring serum biochemical parameters, HE staining, Masson's trichromic staining, and hydroxyproline and α-SMA immunohistochemical staining of liver tissues. The activities of antioxidant enzymes, lipid peroxidation, and Nrf2 signaling pathway-related proteins (Nrf2, Ho-1 and Nqo1) in liver tissues were analyzed. Cultured hepatic stellate cells (HSCs) of rats were prepared for in vitro studies. Results: In the alcohol-and CCl 4 -treated rats, Rg1 administration dose-dependently suppressed the marked increases of serum ALT, AST, LDH and ALP levels, inhibited liver inflammation and HSC activation and reduced liver fibrosis scores. Rg1 significantly increased the activities of antioxidant enzymes (SOD, GSH-Px and CAT) and reduced MDA levels in liver tissues. Furthermore, Rg1 significantly increased the expression and nuclear translocation of Nrf2 that regulated the expression of many antioxidant enzymes. Treatment of the cultured HSCs with Rg1 (1 μmol/L) induced Nrf2 translocation, and suppressed CCl 4 -induced cell proliferation, reversed CCl 4-induced changes in MDA, GPX, PCIII and HA contents in the supernatant fluid and α-SMA expression in the cells. Knockdown of Nrf2 gene diminished these actions of Rg1 in CCl 4 -treated HSCs in vitro. Conclusion: Rg1 exerts protective effects in a rat model of alcohol-and CCl 4 -induced hepatic fibrosis via promoting the nuclear translocation of Nrf2 and expression of antioxidant enzymes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Nrf2 pathway activation contributes to anti-fibrosis effects of ginsenoside Rg1 in a rat model of alcohol- and CCl4-induced hepatic fibrosis

Gao

Chu

et al. 2014

Acta Pharmacol Sin

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“…Previous studies have proved that Panax notoginseng saponin inhibits platelet aggregation in the patients with blood hyperviscosity syndrome (4) and improves I/R-induced hepatic microcirculation disturbance and vascular endothelium function (54), and notoginsenoside R1 inhibits leukocyte rolling and adhesion by inhibiting the expression of adhesion molecules in neutrophils (24). However, which compounds from PN extract corresponding to neuroprotective property in ischemic brain had not been elucidated; it is significant that PN extract reduces the infarction in ischemic brain and inhibits inflammation by activated microglia.…”

Section: Discussionmentioning

confidence: 99%

Panax notoginseng Attenuates the Infarct Volume in Rat Ischemic Brain and the Inflammatory Response of Microglia

et al. 2009

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Abstract. The roots of Panax notoginseng (PN) are commonly used as a therapeutic agent to stop hemorrhage and as a tonic to promote health in traditional Korean medicine. Stroke triggers an inflammatory response that not only plays a central role in the pathogenesis of cerebral ischemia, but also induces secondary damage. This study was designed to investigate the neuroprotective effects of the methanol extract of PN on the infarct volume induced by middle cerebral artery occlusion (MCAO) (90-min occlusion and 24-h reperfusion) in rat brains. The PN extract (50 mg/ kg, i.p.) was administered 2 h after the onset of MCAO. The PN-treated groups had a reduction in infarct volume by 23.82 ± 8.9%. In the PN extract-treated groups, the microglial density was significantly decreased in the peri-infarct region; the underlying mechanism was inhibition of inflammatory mediators, such as inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, via blocking of the NF-κB pathway. Furthermore, in vitro studies showed that the PN extract significantly reduced the production of iNOS-derived NO and COX-2-derived prostaglandin E 2 through the regulation of gene transcription levels in primary microglia and BV-2 cells. These results suggest that anti-inflammatory and microglial activation inhibitory effects of the PN extract may contribute to its neuroprotective effects in brain ischemia.

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“…F.H. Chen (Araliaceae) (Sanqi or Tianqi in Chinese) is a highly valuable and important herb in Oriental traditional medicine for its therapeutic abilities to stop hemorrhaging and to influence blood circulation; it is also the most common drug used to treat chronic liver disease in Korea (2)(3)(4)(5)(6)(7). The main root of P. notoginseng, called notoginseng, is also known to have many pharmacological activities such as anti-inflammatory and anti-tumor effects and it is also known to alter the functional balance of the immune system (8,9).…”

Section: Introductionmentioning

confidence: 99%

Induction of apoptosis in human lung carcinoma cells by the water extract of Panax notoginseng is associated with the activation of caspase-3 through downregulation of Akt

Yoo¹,

Park²,

Cho³

et al. 2009

Int J Oncol

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Abstract. The root of Panax notoginseng is highly valued and commonly used in Oriental medicine. Although recent experimental data have revealed the proapoptotic potency of P. notoginseng extracts, the underlying molecular mechanisms of this apoptotic activity have not yet been studied in detail. In the present study, the effects of the water extract of P. notoginseng (WEPN) on the growth of human lung carcinoma cells were investigated. It was found that the exposure of A549 and NIC-H460 cells to WEPN resulted in growth inhibition and the induction of apoptosis in a dosedependent manner. The WEPN treatment induced the upregulation of pro-apoptotic Bax, downregulation of antiapoptotic Bcl-2 expression and loss of mitochondrial membrane potential (MMP), which was associated with the proteolytic activation of caspases and the concomitant degradation of poly(ADP ribose) polymerase (PARP) protein. However, the caspase-3-specific inhibitor z-DEVD-fmk blocked PARP degradation and increased the survival rate of WEPN-treated cells. Moreover, the activity of Akt was downregulated in WEPN-treated cells and the phosphatidylinositol-3 kinase (PI3K)/Akt inhibitor LY294002 sensitized the cells to WEPN-induced apoptosis through enhancing the activation of caspase-3 and loss of MMP. The results indicated that the major regulators of WEPN-induced apoptosis in human lung carcinoma cells are the Bcl-2 family and caspase-3, which are associated with mitochondrial dysfunction and dephosphorylation of the Akt signaling pathway.

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A Korean herbal medicine, Panax notoginseng, prevents liver fibrosis and hepatic microvascular dysfunction in rats

Cited by 60 publications

References 42 publications

Nrf2 pathway activation contributes to anti-fibrosis effects of ginsenoside Rg1 in a rat model of alcohol- and CCl4-induced hepatic fibrosis

Nrf2 pathway activation contributes to anti-fibrosis effects of ginsenoside Rg1 in a rat model of alcohol- and CCl4-induced hepatic fibrosis

Panax notoginseng Attenuates the Infarct Volume in Rat Ischemic Brain and the Inflammatory Response of Microglia

Induction of apoptosis in human lung carcinoma cells by the water extract of Panax notoginseng is associated with the activation of caspase-3 through downregulation of Akt

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