Panax notoginseng saponins inhibit ischemia-induced apoptosis by activating PI3K/Akt pathway in cardiomyocytes

Chen, Shaoxian; Liu, Juli; Li, Xiaoying; Fu, Yong-Heng; Zhang, Mengzhen; Lin, Qiaoli; Zhu, Ji-Xiao; Mai, Liping; Shan, Zhi‐Xin; Yu, Xiang; Yang, Min; Lin, Shu

doi:10.1016/j.jep.2011.05.011

Cited by 95 publications

(58 citation statements)

References 29 publications

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“…Impairment of ventricular function is the most common fatal complication secondary to ischemic heart diseases. Therefore, improvement of cardiac function and attenuation of ventricular dilation are vital for the treatment of ischemic heart diseases [17]. The present study demonstrated that BA, especially the high dose of BA (200 mg/kg), could increase LVSP, HR, and ± dp / dt max⁡ but decrease LVEDP (Table 1 and Figure 1).…”

Section: Discussionsupporting

confidence: 53%

“…The family consists of both cell death promoters such as Bax and Bad and cell death inhibitors, which include Bcl-2 and Bcl-X. It has been demonstrated that the high ratio of Bax/Bcl-2 is associated with greater vulnerability to apoptotic activation [17, 23–26]. The balance between proapoptotic and antiapoptotic proteins determines the possibility of cells to either survive or undergo apoptosis after a certain stimulus or injury [27].…”

Section: Discussionmentioning

confidence: 99%

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Cardioprotective Effect of Betulinic Acid on Myocardial Ischemia Reperfusion Injury in Rats

Xia

Xue

et al. 2014

Evidence-Based Complementary and Alternative Medicine

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Objectives. This study aims to investigate the effect of betulinic acid (BA) on myocardial ischemia reperfusion/injury in an open-chest anesthetized rat model. Methods. The model was induced by 30 minutes left anterior descending occlusion followed by 2 hours reperfusion. There are six groups in our present study: sham operation group, ischemia/reperfusion group, low-dosage BA group, medium-dosage BA group, high-dosage BA group, and fosinopril sodium group. Rats in the latter four groups were administrated with BA (50, 100, and 200 mg/kg, i.g.) or fosinopril sodium (10 mg/kg, i.g.) once a day for 7 days before operation, respectively. Rats in the former two groups were given the same volume of vehicle (0.5% CMC-Na, i.g.). During the operation, cardiac function was continuously monitored. Serum LDH and CK were measured with colorimetric assays. The expression of Bcl-2 and Bax and the apoptosis of cardiomyocytes were investigated with western blot and TUNEL assay, respectively. Results. Pretreatment with BA improved cardiac function and attenuated LDH and CK activities compared with IR group. Further investigation demonstrated that the expression of Bcl-2 and Bax and TUNEL assay was in line with the above results. Conclusion. BA may reduce the release of LDH and CK, prevent cardiomyocytes apoptosis, and eventually alleviate the extent of the myocardial ischemia/reperfusion injury.

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Section: Discussionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Cardioprotective Effect of Betulinic Acid on Myocardial Ischemia Reperfusion Injury in Rats

Xia

Xue

et al. 2014

Evidence-Based Complementary and Alternative Medicine

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“…This effect might be due to the potential antioxidant and free radical scavenging activities of PG. Also, these antioxidant and radical scavenge activities, and other effects such as antidiabetogenic, antiapoptotic, and immunomodulator activities of PG in pancreas, heart, liver, kidney, and blood tissues, have been demonstrated (Amin et al, 2011;Chen et al, 2011;Karakus et al, 2011;Liu et al, 2010).…”

Section: +mentioning

confidence: 99%

Protective effect of Panax ginseng against N-acetyl-p-aminophenol-induced hepatotoxicity in rats

Uzkeser¹

2012

Afr. J. Pharm. Pharmacol.

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Panax ginseng (PG) has been commonly used as medicinal herb for the treatment of various diseases in Eastern Asia for thousands of years. This study was designed to investigate the protective effect of PG against paracetamol-(N-acetyl-p-aminophenol; APAP)-induced liver damage in rats. Thirty-two albino Wistar rats were divided into four groups: Group C (control); Group APAP (gavaged orally with APAP (APAP, 2 g/kg, single dose); Group PG 100 mg/kg + APAP or 200 mg/kg + APAP (these two groups were treated by gavaging with PG (100 or 200 mg/kg) for 30 days following a single dose of APAP). APAP treatment alone induced hepatotoxicity, evidenced by significant increases in malondialdehyde (MDA) level and serum activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and tumor necrosis factor-α (TNF-α). In addition, the level of GSH in the liver was significantly reduced, as were the activities of superoxide dismutase (SOD) and catalase (CAT). Liver histopathological examination showed that APAP administration induced centrilobular necrosis and infiltration of lymphocytes. However, these biochemical and histological changes were prevented by PG pretreatment. In conclusion, our results suggest that PG may be considered a protective medicinal herb against APAP-induced liver injury.

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“…Panax notoginseng has effects of hemostasis, promoting blood circulation and relieving pain. Recent researches have showed that PNS has pharmacological actions of dilating vessels, decreasing myocardial oxygen consumption, inhibiting platelet aggregation, prolonging blood coagulation time, reducing blood fat, removing free radical, anti-inflammation and antioxidant, and showing cardioprotective effect and neuroprotective effects [8][9][10][11][12][13][14]. Our research focuses on protective effect and anti-inflammatory effect of PNS injection in recovery stage after hemorrhagic shock.…”

Section: Introductionmentioning

confidence: 99%

Protective Mechanism of Panax notoginseng Saponins on Rat Hemorrhagic Shock Model in Recovery Stage

Liu

Zhao

et al. 2014

Cell Biochem Biophys

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To explore protective mechanism of Panax notoginseng saponins (PNS) on rat hemorrhagic shock model in recovery stage. 72 Wistar rats were selected and divided into control group, model group and PNS group with 24 rats in each group. 200 mg/kg PNS was injected intravenously at 60 min of hemorrhagic shock stage in PNS groups. Changes of endotoxin, MPO, IL-6, SOD, MDA and TNF α were observed at 30 and 120 min of recovery stage by ELISA; water content of lung and intestine was detected; HE staining was applied to observe morphological change of intestinal mucosa, kidney, liver and lung; western blot was used to detect intercellular adhesion molecule-1 (ICAM-1) level in lung tissue and intestine tissue. At 30 min and 120 min of recovery stage, MDA, MPO, endotoxin, TNF α and IL-6 levels significantly increased in model group compared with control group, however SOD level significantly decreased, the difference was statistically significant (P < 0.05); PNS dose-dependently decreased MDA, MPO, endotoxin, TNF α and IL-6 levels, and increased SOD level, which was statistically significant (P < 0.05); In results of water content detection, water content in lung tissue and intestine tissue was significantly higher than in control group, however, after being treated with PNS, the water content was significantly decreased; HE staining showed the morphologic change of lung tissue cells; Western blot showed that in lung tissue and intestine tissue, ICAM-1 level in model group was significantly higher than in control group, and it was lower in PNS group than in model group. PNS can increase SOD activity, decrease levels of MDA, endotoxin and MPO, decrease expression of TNF α and IL-6, and decrease water content in lung tissue and intestine tissue. Thus, PNS is protective to rat hemorrhagic shock model by anti oxidative stress and anti-inflammatory pathways, and ICAM-1 may play an important role in the mechanism.

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Panax notoginseng saponins inhibit ischemia-induced apoptosis by activating PI3K/Akt pathway in cardiomyocytes

Cited by 95 publications

References 29 publications

Cardioprotective Effect of Betulinic Acid on Myocardial Ischemia Reperfusion Injury in Rats

Cardioprotective Effect of Betulinic Acid on Myocardial Ischemia Reperfusion Injury in Rats

Protective effect of Panax ginseng against N-acetyl-p-aminophenol-induced hepatotoxicity in rats

Protective Mechanism of Panax notoginseng Saponins on Rat Hemorrhagic Shock Model in Recovery Stage

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