Biochanin A attenuates myocardial ischemia/reperfusion injury through the TLR4/NF-κB/NLRP3 signaling pathway

Bai, Yejun; Li, Zhigang; Liu, Weihao; Gao, Dong; Liu, Min; Zhang, Peiying

doi:10.1590/s0102-865020190110000004

Cited by 58 publications

(39 citation statements)

References 38 publications

(33 reference statements)

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“…However, only the expressions of BAFF, BAFF-R, IL-1b, and IL-8 were changed rather than C1GALT1 and Cosmc when knocking down the expression of TLR4 ( Figure 5 and Supplemental Figure 2). Previous studies had demonstrated that the expressions of IL-1b and IL-8 could regulate the concentration of IgA and TLR4/NF-kB axis could modulate the expression of IL-1b and IL-8 (42)(43)(44). In present study, we also found that overexpression of TLR4 could active the NF-kB p65 signaling pathway.…”

Section: Discussionsupporting

confidence: 77%

microRNA-630 Regulates Underglycosylated IgA1 Production in the Tonsils by Targeting TLR4 in IgA Nephropathy

Liu

Yan

et al. 2020

Front. Immunol.

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IgA nephropathy (IgAN) is the most common primary glomerular disease. The characteristic pathology involves immune complexes formed by the deposition of IgA1 and underglycosylated IgA1 aggregates in the mesangial area, which may be accompanied by the deposition of IgG and/or IgM and complement components. However, the molecular mechanisms of IgAN remain unclear. In the present study, microarray analysis showed that the expression of microRNA-630 (miR-630) was significantly reduced in palatal tonsils from IgAN patients compared with chronic tonsillitis. Additionally, bioinformatic analysis showed that Toll-like receptor 4 (TLR4) was the predicted target gene of miR-630 and was regulated by miR-630. When miR-630 was overexpressed in palatal tonsil mononuclear cells from IgAN patients, the expression of TLR4 was reduced and the content of IgA1 in the cell culture supernatant was decreased, and the level of galactosylation in the IgA1 hinge region was increased. Moreover, immunohistochemical analysis showed that the expression of TLR4 in IgAN patients was significantly increased. After knocking down the expression of TLR4, both the concentration of IgA1 and the binding force of IgA1 with broad bean lectin were significantly reduced in IgAN. Furthermore, the mechanism study demonstrated that TLR4 might regulate the expression of IL-1β and IL-8 through NF-κB signaling pathway to modulate the concentration of IgA1 and the glycosylation level of IgA1. This interesting finding may offer new insight into the molecular mechanism of IgAN.

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Section: Discussionsupporting

confidence: 77%

microRNA-630 Regulates Underglycosylated IgA1 Production in the Tonsils by Targeting TLR4 in IgA Nephropathy

Liu

Yan

et al. 2020

Front. Immunol.

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“…Studies have proved that many flavonoids possessed unique antioxidants and protection against myocardial I/R injury [45][46][47]. Kaempferol, a naturally occurring flavonoid, also has a very good antioxidant, anti-inflammatory, and cardioprotective properties in myocardial I/R injury [11,12].…”

Section: Plos Onementioning

confidence: 99%

MiR-21 mediates the protection of kaempferol against hypoxia/reoxygenation-induced cardiomyocyte injury via promoting Notch1/PTEN/AKT signaling pathway

Huang

2020

PLoS ONE

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Kaempferol, a natural flavonoid compound, possesses potent myocardial protective property in ischemia/reperfusion (I/R), but the underlying mechanism is not well understood. The present study was aimed to explore whether miR-21 contributes to the cardioprotective effect of kaempferol on hypoxia/reoxygenation (H/R)-induced H9c2 cell injury via regulating Notch/phosphatase and tensin homologue (PTEN)/Akt signaling pathway. Results revealed that kaempferol obviously attenuates H/R-induced the damages of H9c2 cells as evidence by the up-regulation of cell viability, the down-regulation of lactate dehydrogenase (LDH) activity, the reduction of apoptosis rate and pro-apoptotic protein (Bax) expression, and the increases of anti-apoptotic protein (Bcl-2) expression. In addition, kaempferol enhanced miR-21 level in H9c2 cells exposed to H/R, and inhibition of miR-21 induced by transfection with miR-21 inhibitor significantly blocked the protection of kaempferol against H/R-induced H9c2 cell injury. Furthermore, kaempferol eliminated H/R-induced oxidative stress and inflammatory response as illustrated by the decreases in reactive oxygen species generation and malondialdehyde content, the increases in antioxidant enzyme superoxide dismutase and glutathione peroxidase activities, the decreases in pro-inflammatory cytokines interleukin (IL)-1β, IL-8 and tumor necrosis factor-alpha levels, and an increase in anti-inflammatory cytokine IL-10 level, while these effects of kaempferol were all reversed by miR-21 inhibitor. Moreover, results elicited that kaempferol remarkably blocks H/R-induced the down-regulation of Notch1 expression, the up-regulation of PTEN expression, and the reduction of P-Akt/Akt, indicating that kaempferol promotes Notch1/PTEN/AKT signaling pathway, and knockdown of Notch1/PTEN/AKT signaling pathway induced by Notch1 siRNA also abolished the protection of kaempferol against H/R-induced the damage of H9c2 cells. Notably, miR-21 inhibitor alleviated the promotion of kaempferol on Notch/PTEN/Akt signaling pathways in H9c2 cells exposed to H/R. Taken together, these above findings suggested thatmiR-21 mediates the protection of kaempferol against H/R-induced H9c2 cell injuryvia promoting Notch/PTEN/Akt signaling pathway.

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“…To determine the mechanism of drug action, the classic in ammation-related TLR4/NF-κB signaling pathway was assayed. Bai Y. et al determined that biochanin A attenuates myocardial ischemia-reperfusion injury via the TLR4/NF-kappaB/NLRP3 signaling pathway [14]. HuaSheng D. et al determined that the HMGB1-TLR4 axis participates in myocardial ischemia-reperfusion injury by regulating myocardial cell apoptosis [22].…”

Section: Discussionmentioning

confidence: 99%

“…Biochanin A can reduce the levels of IL-1β, IL-18, IL-6, and TNF-α in the serum, inhibit the expression of related proteins TLR4, MyD88, NLRP3, ASC, and caspase-1, and inhibit the phosphorylation of IkB-α and NF-κB to suppress in ammation through the TLR4/NF-κB signaling pathway and thus protect the myocardium [14]. Luteolin protects cardiomyocytes from ischemia-reperfusion injury via the TLR4/NF-κB/NLRP3 pathway [15].…”

Section: Tlr4/nf-κb Signaling Pathwaymentioning

confidence: 99%

The Protective Effect of Shuxin Shengmai Dan on Myocardial Ischemia-Reperfusion Injury in Rats

Wang¹,

Hao²,

Piao³

et al. 2020

Preprint

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Background: The traditional Chinese medicine Shuxin Shengmai Dan (SXSMD) is clinically used to treat angina pectoris. The mechanism of action of SXSMD protection of the heart involves inhibition of inflammation and remains poorly understood. The role of SXSMD in rats with myocardial ischemia reperfusion (IR) and the mechanism of SXSMD action were studied in this research.Methods: The rats were treated with SXSMD (3.38, 6.76, and 13.52 g/kg/day, p.o.) or Danshen injecta (1.8 mL/kg/day, p.o.) for 15 days, then the coronary arteries were ligated. Cardiac function was evaluated by electrocardiography and hemodynamic measurements. Hematoxylin-eosin (H&E) staining was used to detect pathological changes in ischemic myocardial sections. Transmission electron microscopy (TEM) was used to assess the ultrastructure of cardiomyocytes. The changes in IL-6 and TNF-α in the rat serum were detected by ELISA. The changes in the expression levels of HMGB1, TLR4, MyD88, and NF-κB mRNAs and proteins related to the TLR4/NF-κB pathway in myocardial tissue were detected by qPCR and Western blot, respectively.Results: Rats with coronary artery ligation had abnormal cardiac function, inflammatory infiltration of myocardial cells, disordered myocardial fiber arrangement, accumulation of mitochondria, and disordered muscle fibers and sarcomeres according to electron microscopy. The levels of the expression of mRNAs and proteins in myocardial tissue of the SXSMD group were decreased compared with those in the MIRI group. The serum levels of IL-6 and TNF-α were decreased. SXSMD treatment can inhibit the inflammatory response and downregulate the TLR4/NF-κB pathway in cardiomyocytes.Conclusion: SXSMD protects the rats from myocardial ischemia-reperfusion injury in the MIRI model by downregulating the TLR4/NF-κB pathway to inhibit inflammation.

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Biochanin A attenuates myocardial ischemia/reperfusion injury through the TLR4/NF-κB/NLRP3 signaling pathway

Cited by 58 publications

References 38 publications

microRNA-630 Regulates Underglycosylated IgA1 Production in the Tonsils by Targeting TLR4 in IgA Nephropathy

microRNA-630 Regulates Underglycosylated IgA1 Production in the Tonsils by Targeting TLR4 in IgA Nephropathy

MiR-21 mediates the protection of kaempferol against hypoxia/reoxygenation-induced cardiomyocyte injury via promoting Notch1/PTEN/AKT signaling pathway

The Protective Effect of Shuxin Shengmai Dan on Myocardial Ischemia-Reperfusion Injury in Rats

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