Huang Qi Tong Bi Decoction Attenuates Myocardial Ischemia-Reperfusion Injury via HMGB1/TLR/NF-<i>κ</i>B Pathway

Liu, Kun; Li, Manman; Ren, Xiumei; You, Qingsheng; Wang, Fei; Wang, Shuo; Ma, Chunhui; Li, Weinan; Ye, Qing

doi:10.1155/2019/8387636

Cited by 14 publications

(15 citation statements)

References 16 publications

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“…According to our previous report [10], each healthy SD male rat was carefully weighed and prepared to undergo an intraperitoneal injection (0.5 ml/100 mg) of ethyl carbamate, subject to effective anesthesia. After the rats were successfully anesthetized, the rats were fixed on the operating table in supine position and the rats were carefully connected to a standard lead electrocardiogram instrument to monitor whether the operation indexes were abnormal.…”

Section: Methodsmentioning

confidence: 99%

“…According to our previous report [10], taking H9c2 cells growing in the logarithmic growth phase to discard the original culture solution and replace it with anoxic solution saturated with 95% N 2 and 5% CO 2 mixed gas in advance, placing the culture plate in a sealed container (37°C) with 95% N 2 and 5% CO 2 continuous aeration for 6 h to obtain anoxic solution, replacing the anoxic solution with reoxygenation solution saturated with 95% O 2 and 5% CO 2 mixed gas in advance, and placing it in a CO 2 incubator (5% CO 2 , 95% air, and 37°C temperature) for reoxygenation culture to obtain reoxygenation were carried out.…”

Section: Methodsmentioning

confidence: 99%

“…According to our previous report [10], H9c2 cardiomyocytes were seeded on a 96-well plate 1 × 10 4 /well. After 6 hours of hypoxia treatment, cells were cultured for 24 hours after reoxidation according to the instructions of the CCK8 detection kit.…”

Section: Methodsmentioning

confidence: 99%

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Mangiferin Attenuates Myocardial Ischemia-Reperfusion Injury via MAPK/Nrf-2/HO-1/NF-κB In Vitro and In Vivo

Liu

Wang

et al. 2019

Oxidative Medicine and Cellular Longevity

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The aim of this study was to investigate the cardioprotective effect of mangiferin (MAF) in vitro and in vivo. Oxidative stress and inflammatory injury were detected in coronary artery ligation in rats and also in hypoxia-reoxygenation- (H/R-) induced H9c2 cells. MAF inhibited myocardial oxidative stress and proinflammatory cytokines in rats with coronary artery occlusion. The ST segment of MAF treatment groups also resumed. Triphenyltetrazolium chloride (TTC) staining and pathological analysis showed that MAF could significantly reduce myocardial injury. In vitro data showed that MAF could improve hypoxia/reoxygenation- (H/R-) induced H9c2 cell activity. In addition, MAF could significantly reduce oxidative stress and inflammatory pathway protein expression in H/R-induced H9c2 cells. This study has clarified the protective effects of MAF on myocardial injury and also confirmed that oxidative stress and inflammation were involved in the myocardial ischemia-reperfusion injury (I/R) model.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Mangiferin Attenuates Myocardial Ischemia-Reperfusion Injury via MAPK/Nrf-2/HO-1/NF-κB In Vitro and In Vivo

Liu

Wang

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…By blocking the TLR4 recognition signal, the inflammation signal cannot be passed into the cell, thus inhibiting the activity of NF-κB and inflammation. Therefore, the HMGB1/TLR4/NF-κB inflammation cascade is an important pathway leading to the activation of the inflammatory response [30].…”

Section: Introductionmentioning

confidence: 99%

Salvianolic Acid D Alleviates Cerebral Ischemia-Reperfusion Injury by Suppressing the Cytoplasmic Translocation and Release of HMGB1-Triggered NF-κB Activation to Inhibit Inflammatory Response

Zhang

Song

Wan

et al. 2020

Mediators of Inflammation

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Inflammatory response participates in the overall pathophysiological process of stroke. It is a promising strategy to develop antistroke drugs targeting inflammation. This study is aimed at investigating the therapeutic effect and anti-inflammatory mechanism of salvianolic acid D (SalD) against cerebral ischemia/reperfusion (I/R) injury. A rat middle cerebral artery occlusion/reperfusion (MCAO/R) injury model was established, and an oxygen-glucose deprivation/reoxygenation (OGD/R) injury model was established in PC12 cells. Neurological deficit score, cerebral infarction, and edema were studied in vivo. Cell viability was achieved using the MTT method in vitro. The Bax, Bcl-2, cytochrome c, HMGB1, TLR4, TRAF6, NF-κB p65, p-NF-κB p65, and cleaved caspase-3 and -9 were tested via the Western blot method. Cytokines and cytokine mRNA, including TNF-α, IL-1β, and IL-6, were studied via ELISA and PCR methods. The translocation of HMGB1 and NF-κB were studied by immunofluorescence assay. The HMGB1/NeuN, HMGB1/GFAP, and HMGB1/Iba1 double staining was carried out to observe the localization of HMGB1 in different cells. Results showed that SalD alleviated neurological impairment, decreased cerebral infarction, and reduced edema in I/R rats. SalD improved OGD/R-downregulated PC12 cell viability. SalD also promoted Bcl-2 expression and suppressed Bax, cytochrome c, and cleaved caspase-3 and -9 expression. SalD decreased the intensity of TLR4, MyD88, and TRAF6 proteins both in vivo and in vitro, and significantly inhibited the NF-κB nuclear translocation induced by I/R and OGD/R. What’s more, SalD inhibited HMGB1 cytoplasmic translocation in neurons, astrocytes, and microglia in both the cortex and hippocampus regions of I/R rats. In conclusion, SalD can alleviate I/R-induced cerebral injury in rats and increase the PC12 cell viability affected by OGD/R. The anti-inflammatory mechanism of SalD might result from the decreased nuclear-to-cytoplasmic translocation of HMGB1 and the inhibition on its downstream TLR4/MyD88/NF-κB signaling.

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“…Following BP measurements, blood samples from diferent eperimental groups were collected from the left ventricle, centrifuged (20 min/4,000 rpm) and the detached serum was kept in −80°C deep freezer, for the subsequent biochemical investigations. Animals' hearts were rapidly separated, washed with saline, weighed and freezed (−20°C) as mentioned in earlier report [26].…”

Section: Heart To Body Ratio Determentation and Sample Processingmentioning

confidence: 99%

D-Limonene mitigate myocardial injury in rats through MAPK/ERK/NF-κB pathway inhibition

Younis

2020

Korean J Physiol Pharmacol

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Cardiovascular diseases are the primary reason of mortality, among which myocardial infarction (MI) is the most dominant and prevalent. This study was considered to examine D-Limonene protective action against isoproterenol (ISO) induced MI. Wister male rats were dispersed into four groups. Normal and D-Limonene control group in which rats administered saline or D-Limonene. ISO control animals were administered saline for 21 days then challenged with ISO (85 mg/kg, subcutaneously) on 20th and 21st day for MI induction. D-Limonene pretreated group in which animals were pretreated with D-Limonene 50 mg/kg orally for 21 days then administered ISO on 20th and 21st day. MI prompted variations were assessed by myocardial infarction area determination, blood pressure (BP) alterations, cardiac injury biomarkers and inflammatory mediators measurements. For more depth investigation, both the apoptotic status was evaluated via measuring mRNA expression of Bcl-2 and Bax as well as mitogen-activated protein kinase-extracellular signal-regulated kinase (MAPK-ERK) signal transduction were investigated via Western blotting. MI group revealed significant infarcted area, blood pressure alterations, myocardial injury enzymes intensification together with inflammatory cytokines amplification. MI was associated with activation of MAPK-ERK signal pathway and apoptotic status within the myocardium. On the other hand, pretreated with D-Limonene demonstrated deterred infracted area, reduced myocardial enzymes, improved BP indices, lessened inflammatory levels. Furthermore, D-Limonene pretreatment caused a decline in MAPK proteins pathway and Bax relative mRNA expression, while intensifying Bcl-2 mRNA expression promoting that D-Limonene may constrain MI induced myocardial apoptosis. D-Limonene mitigated MI injury through MAPK/NF-κB pathway inhibition and anti-apoptotic effect.

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Huang Qi Tong Bi Decoction Attenuates Myocardial Ischemia-Reperfusion Injury via HMGB1/TLR/NF-κB Pathway

Cited by 14 publications

References 16 publications

Mangiferin Attenuates Myocardial Ischemia-Reperfusion Injury via MAPK/Nrf-2/HO-1/NF-κB In Vitro and In Vivo

Mangiferin Attenuates Myocardial Ischemia-Reperfusion Injury via MAPK/Nrf-2/HO-1/NF-κB In Vitro and In Vivo

Salvianolic Acid D Alleviates Cerebral Ischemia-Reperfusion Injury by Suppressing the Cytoplasmic Translocation and Release of HMGB1-Triggered NF-κB Activation to Inhibit Inflammatory Response

D-Limonene mitigate myocardial injury in rats through MAPK/ERK/NF-κB pathway inhibition

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