Ginsenoside Rg3 Improves Cardiac Function after Myocardial Ischemia/Reperfusion via Attenuating Apoptosis and Inflammation

Zhang, Liping; Jiang, Yichuan; Yu, Xiaofeng; Xu, Huali; Li, Min; Zhao, Xin

doi:10.1155/2016/6967853

Cited by 68 publications

(42 citation statements)

References 21 publications

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“…These proinflammatory cytokines not only injure cardiac tissue locally, but also are released into the circulatory system leading to systemic injury [ 26 , 27 ]. Therefore, a reduction of the levels of TNF-a and IL-6 could alleviate MIRI [ 7 , 28 , 29 ].…”

Section: Discussionmentioning

confidence: 99%

6‐Gingerol Protects Heart by Suppressing Myocardial Ischemia/Reperfusion Induced Inflammation via the PI3K/Akt‐Dependent Mechanism in Rats

Qin

Jiang

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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Our previous study has demonstrated that 6-Gingerol (6-G) could alleviate myocardial ischemia/reperfusion injury (MIRI). However, the molecular mechanism underlying the process of myocardial ischemia/reperfusion (I/R) injury alleviation by 6-G remains unelucidated. The objective of the present study is to further investigate the potential mechanism for 6-G to alleviate MIRI in rats. Thirty-two Sprague-Dawley rats were randomly divided into four groups: the Sham group, the I/R group, the 6-G + I/R group, and the LY294002 (LY) + 6-G + I/R group. For the rats in each of the groups, data were collected for cardiogram, cardiac function, area of myocardial infarction, myocardial pathology, myocardial enzyme, marker of inflammatory response, and PI3K/Akt signaling pathway. We found that the pretreatment of 6-G with 6 mg/kg could shrink the ST section of cardiogram, improve the cardiac function, reduce the area of myocardial infarction and the degree of cardiac pathological injury, lower the level of myocardial enzyme, and inhibit the inflammatory response. In addition, our results also indicated that 6-G could upregulate the expression of PI3K and p-Akt and that LY294002, a blocking agent of PI3K/Akt signaling pathway, could nullify the protecting role of 6-G. Our experimental results showed that 6-G could inhibit I/R-induced inflammatory response through the activation of the PI3K/Akt signaling pathway.

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Section: Discussionmentioning

confidence: 99%

6‐Gingerol Protects Heart by Suppressing Myocardial Ischemia/Reperfusion Induced Inflammation via the PI3K/Akt‐Dependent Mechanism in Rats

Qin

Jiang

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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“…On the first and last days of the 6-week treatment, transthoracic echocardiography was performed as previously described ( 23 ), using a standard setting with a 10S transducer (Vivid-i; GE Healthcare, Chicago, IL, USA). Animals were anesthetized with chloral hydrate (300 mg/kg, intraperitoneally) and two-dimensional and M-mode echocardiographic measurements were conducted.…”

Section: Methodsmentioning

confidence: 99%

Ginsenoside Rg3 induces ginsenoside Rb1-comparable cardioprotective effects independent of reducing blood pressure in spontaneously hypertensive rats

Jiang

et al. 2017

Exp Ther Med

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Ginsenoside Rg3 (Rg3) is a rare type of ginsenoside used as an anti-tumor medicine in China. Ginsenoside Rb1 (Rb1), which exhibits protective effects on the cardiovascular system, is similar to Rg3 in chemical structure. In the present study, Rb1 and Rg3 were administered for 6 weeks to spontaneously hypertensive rats (SHR) and their cardioprotective effects were assessed. According to echocardiography and histopathological examinations, the decrease in cardiac function and ventricular remodeling that occurred in SHR rats were attenuated by Rb1 and Rg3. However, tail-cuff blood pressure measurements indicated that Rb1 and Rg3 did not reduce blood pressure in SHR rats. The cardioprotective effects of Rb1 and Rg3 occurred independently of blood pressure reduction. Furthermore, immunohistochemistry (IHC) revealed that renin angiotensin system (RAS) activity in the myocardium of SHR was significantly attenuated by Rb1 and Rg3, whereas ELISA identified no significant changes of RAS activity in the serum. The results of IHC and reverse transcription-quantitative polymerase chain reaction demonstrated that levels of transforming growth factor β1, tumor necrosis factor-α, interleukin-6, interleukin-1 and endothelian-1 in the myocardium of SHR rats were reduced following Rb1 and Rg3 treatment. This may be due to the attenuation of RAS activity in the myocardium and the mechanisms of the cardioprotective effects of Rb1 and Rg3.

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“…Diverse natural compounds provide beneficial health effects through modulating these targets against excessive and/or aberrant inflammation, oxidative stress, and apoptosis [ 16 – 18 ]. For instance, ginsenosides ameliorate myocardial I/R-induced inflammation, oxidative stress, and apoptosis via inhibiting the p53 pathway [ 19 ]. Berberine ameliorates renal I/R-induced inflammation, mitochondrial dysfunction, oxidative stress, and apoptosis via inhibiting the p53 pathway [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

Cinnamaldehyde protects against rat intestinal ischemia/reperfusion injuries by synergistic inhibition of NF-κB and p53

Almoiliqy

Wen

et al. 2020

Acta Pharmacol Sin

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Our preliminary study shows that cinnamaldehyde (CA) could protect against intestinal ischemia/reperfusion (I/R) injuries, in which p53 and NF-κB p65 play a synergistic role. In this study, we conducted in vivo and in vitro experiments to verify this proposal. SD rats were pretreated with CA (10 or 40 mg · kg −1 · d −1 , ig) for 3 days, then subjected to 1 h mesenteric ischemia followed by 2 h reperfusion. CA pretreatment dose-dependently ameliorated morphological damage and reduced inflammation evidenced by decreased TNF-α, IL-1β, and IL-6 levels and MPO activity in I/R-treated intestinal tissues. CA pretreatment also attenuated oxidative stress through restoring SOD, GSH, LDH, and MDA levels in I/R-treated intestinal tissues. Furthermore, CA pretreatment significantly reduced the expression of inflammation/apoptosis-related NF-κB p65, IKKβ, IK-α, and NF-κB p50, and downregulated apoptotic protein expression including p53, Bax, caspase-9 and caspase-3, and restoring Bcl-2, in I/R-treated intestinal tissues. We pretreated IEC-6 cells in vitro with CA for 24 h, followed by 4 h hypoxia and 3 h reoxygenation (H/R) incubation. Pretreatment with CA (3.125, 6.25, and 12.5 μmol · L −1 ) significantly reversed H/R-induced reduction of IEC-6 cell viability. CA pretreatment significantly suppressed oxidative stress, NF-κB activation and apoptosis in H/R-treated IEC-6 cells. Moreover, CA pretreatment significantly reversed mitochondrial dysfunction in H/R-treated IEC-6 cells. CA pretreatment inhibited the nuclear translocation of p53 and NF-κB p65 in H/R-treated IEC-6 cells. Double knockdown or overexpression of p53 and NF-κB p65 caused a synergistic reduction or elevation of p53 compared with knockdown or overexpression of p53 or NF-κB p65 alone. In H/R-treated IEC-6 cells with double knockdown or overexpression of NF-κB p65 and p53, CA pretreatment caused neither further decrease nor increase of NF-κB p65 or p53 expression, suggesting that CA-induced synergistic inhibition on both NF-κB and p53 played a key role in ameliorating intestinal I/R injuries. Finally, we used immunoprecipitation assay to demonstrate an interaction between p53 and NF-κB p65, showing the basis for CA-induced synergistic inhibition. Our results provide valuable information for further studies.

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Ginsenoside Rg3 Improves Cardiac Function after Myocardial Ischemia/Reperfusion via Attenuating Apoptosis and Inflammation

Cited by 68 publications

References 21 publications

6‐Gingerol Protects Heart by Suppressing Myocardial Ischemia/Reperfusion Induced Inflammation via the PI3K/Akt‐Dependent Mechanism in Rats

6‐Gingerol Protects Heart by Suppressing Myocardial Ischemia/Reperfusion Induced Inflammation via the PI3K/Akt‐Dependent Mechanism in Rats

Ginsenoside Rg3 induces ginsenoside Rb1-comparable cardioprotective effects independent of reducing blood pressure in spontaneously hypertensive rats

Cinnamaldehyde protects against rat intestinal ischemia/reperfusion injuries by synergistic inhibition of NF-κB and p53

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