Salvianolic acid B inhibits the TLR4-NFκB-TNFα pathway and attenuates neonatal rat cardiomyocyte injury induced by lipopolysaccharide

Jie Wang; Yun Zhang; Li-li Guo; Guang-jun Wu; Rui-hua Liu

doi:10.1007/s11655-011-0877-x

Your Location：

Home >

Browse articles >

Salvianolic acid B inhibits the TLR4-NFκB-TNFα pathway and attenuates neonatal rat cardiomyocyte injury induced by lipopolysaccharide

OriginalPaper | Updated：2021-08-27

- Salvianolic acid B inhibits the TLR4-NFκB-TNFα pathway and attenuates neonatal rat cardiomyocyte injury induced by lipopolysaccharide
- Salvianolic acid B inhibits the TLR4-NFκB-TNFα pathway and attenuates neonatal rat cardiomyocyte injury induced by lipopolysaccharide
- 中国结合医学杂志（英文版） 2011年17卷第10期页码：775-779
- Affiliations：
  
  1. Guang’anmen Hospital, China Academy of Chinese Medical Sciences,Beijing,China
  2. Hubei University of Traditional Chinese Medicine,Wuhan,China
- Author bio：
- Funds：
  
  Supported by the Foundation of Guang’anmen Hospital, China Academy of Chinese Medical Sciences (No. 81359)
- DOI：10.1007/s11655-011-0877-x
  中图分类号：
- 纸质出版日期：2011，
  
  网络出版日期：2013-3-26，
Scan for full text
Wang, J., Zhang, Y., Guo, Ll. et al. Salvianolic acid B inhibits the TLR4-NFκB-TNFα pathway and attenuates neonatal rat cardiomyocyte injury induced by lipopolysaccharide., Chin. J. Integr. Med. 17, 775–779 (2011). https://doi.org/10.1007/s11655-011-0877-x

Jie Wang, Yun Zhang, Li-li Guo, et al. Salvianolic acid B inhibits the TLR4-NFκB-TNFα pathway and attenuates neonatal rat cardiomyocyte injury induced by lipopolysaccharide[J]. Chinese Journal of Integrative Medicine, 2011,17(10):775-779.
Wang, J., Zhang, Y., Guo, Ll. et al. Salvianolic acid B inhibits the TLR4-NFκB-TNFα pathway and attenuates neonatal rat cardiomyocyte injury induced by lipopolysaccharide., Chin. J. Integr. Med. 17, 775–779 (2011). https://doi.org/10.1007/s11655-011-0877-x DOI：

Jie Wang, Yun Zhang, Li-li Guo, et al. Salvianolic acid B inhibits the TLR4-NFκB-TNFα pathway and attenuates neonatal rat cardiomyocyte injury induced by lipopolysaccharide[J]. Chinese Journal of Integrative Medicine, 2011,17(10):775-779. DOI： 10.1007/s11655-011-0877-x.

摘要

To investigate the role of the TLR4-NFκB-TNFα inflammation pathway on: lipopolysaccharide (LPS)-induced neonatal rat cardiomyocyte injury and the possible protective effects of salvianolic acid B (Sal B). Wistar rat (1–2 days old) cardiomyocytes were isolated and cultured. Sal B 10−5mol/L

10−6mol/L and 10−7mol/L were pre-treated for 6 h in the culture medium. LPS (1 μg/mL) was added to mol/the culture medium and kept for 6 h to induce inflammation injury. The concentration of lactate dehydrogenase (LDH) in the supernatant was detected by spectrophotometry. The concentrations of tumor necrosis factor α (TNFα) and heat shock protein 70 (HSP70) in the supernatant were detected by enzyme linked immunosorbent assay. The protein expressions of toll

such as receptor 4 (TLR4) and nuclear factor kappa B (NFκB) were detected by immunohistochemistry. The mRNA expressions of TLR4 and NFκB were detected by real-realtime reverse transcription polymerase chain reaction (RT-PCR). (1) The concentrations of LDH and: TNFα in the LPS control group were significantly higher than those in the control group (561.41±67.39 U/L and 77.94±15.08 pg/mL

versus 292.13±26.02 U/L and 25.39±16.53 pg/mL

respectively

P<0.01

P<0.05). Compared with the LPS control group

the concentrations of LDH and TNFα were significantly decreased in the Sal B 10−5mol/L pre-treated group (451.76±83.96 U/L and 34.00±10.38 pg/mL

respectively

P<0.05). (2) The TLR4 and NFκB protein expression area in the LPS control group were significantly higher than those in the control group (1712.41±410.12 μm2 and 2378.15±175.29 μm2

versus 418.62±24.42 μm2 and 1721.74±202.87 μm2

respectively

P<0.01). The TLR4 and NFκB protein expression internal optical density (IOD) values in the LPS control group were also significantly higher than those in the control group (3.06±0.33 and 7.20±1.04

versus 0.91±0.21 and 4.24±0.48

respectively

P<0.05 and P<0.01). Compared with the LPS control group

the TLR4 and NFκB protein expression areas were significantly decreased in the Sal B 10−5mol/L pre-treated group (1251.54±133.82 μm2 and 1996.37±256.67 μm2

respectively

P<0.05)

the TLR4 and NFκB protein expression IOD values were also significantly decreased in the Sal B 10−5mol/L pre- mol/pretreated group (1.92±0.28 and 5.17±0.77

respectively

treated P<0.05). (3) The TLR4 and NFκB mRNA expressions (2−ΔΔCT value) in the LPS control group were significantly higher than those in the control group (3.16±0.38 and 5.03±0.43 versus 1.04±0.19 and 1.08±0.21

respectively

P<0.01). Compared with the LPS control group

the TLR4 and NFκB mRNA expressions (2−ΔΔ -CT value) were significantly decreased in the Sal B 10−5mol/L pre- mol/pretreated group (1.34±0.22 and 1.74±0.26

respectively

treated P<0.05). The concentration of HSP70 did not show any <statistical differences in all groups (P>0.05). The TLR4-NFκB-TNFα pathway was quickly activated: and was independent of HSP70 in the early phase of neonatal cardiomyocyte injury induced by LPS. The protective effects of Sal B may be through inhibiting the TLR4-NFκB-TNFα pathway and are dose-dependent.

Abstract

versus 292.13±26.02 U/L and 25.39±16.53 pg/mL

respectively

P<0.01

P<0.05). Compared with the LPS control group

the concentrations of LDH and TNFα were significantly decreased in the Sal B 10−5mol/L pre-treated group (451.76±83.96 U/L and 34.00±10.38 pg/mL

respectively

P<0.05). (2) The TLR4 and NFκB protein expression area in the LPS control group were significantly higher than those in the control group (1712.41±410.12 μm2 and 2378.15±175.29 μm2

versus 418.62±24.42 μm2 and 1721.74±202.87 μm2

respectively

P<0.01). The TLR4 and NFκB protein expression internal optical density (IOD) values in the LPS control group were also significantly higher than those in the control group (3.06±0.33 and 7.20±1.04

versus 0.91±0.21 and 4.24±0.48

respectively

P<0.05 and P<0.01). Compared with the LPS control group

the TLR4 and NFκB protein expression areas were significantly decreased in the Sal B 10−5mol/L pre-treated group (1251.54±133.82 μm2 and 1996.37±256.67 μm2

respectively

P<0.05)

the TLR4 and NFκB protein expression IOD values were also significantly decreased in the Sal B 10−5mol/L pre- mol/pretreated group (1.92±0.28 and 5.17±0.77

respectively

P<0.01). Compared with the LPS control group

the TLR4 and NFκB mRNA expressions (2−ΔΔ -CT value) were significantly decreased in the Sal B 10−5mol/L pre- mol/pretreated group (1.34±0.22 and 1.74±0.26

respectively

关键词

salvianolic acid BTLR4-NFκB-TNFα pathwaycardiomyocyteslipopolysaccharide

Keywords

salvianolic acid BTLR4-NFκB-TNFα pathwaycardiomyocyteslipopolysaccharide

references

Li X, Li Y, Shan L, Chen R, Peng T. Over-expression of calpastatin inhibits calpain activation and attenuates myocardial dysfunction during endotoxaemia. Cardiovasc Res 2009;83:72–79.

da Silveira Cruz-Machado S, Carvalho-Sousa CE, Tamura EK, Pinato L, Cecon E, Fernandes PA, de Avellar MC, et al. TLR4 and CD14 receptors expressed in rat pineal gland trigger NFκB pathway. J Pineal Res 2010;49:183–192.

Mong PY, Petrulio C, Kaufman HL, Wang Q. Activation of Rho kinase by TNF-alpha is required for JNK activation in human pulmonary microvascular endothelial cells. J Immunol 2008;180:550–558.

Wu HL, Li YH, Lin YH, Wang R, Li YB, Tie L, et al. Salvianolic acid B protects human endothelial cells from oxidative stress damage: a possible protective role of glucose-regulated protein 78 induction. Cardiovasc Res 2009;81:148–158.

Chen YH, Lin SJ, Chen YL, Liu PL, Chen JW. Anti- inflammatory effects of different drugs/agents with antioxidant property on endothelial expression of adhesion molecules. Cardiovasc Hematological Disord Drug Targets 2006;6:279–304.

Wang SX, Hu LM, Gao XM, Guo H, Fan GW. Anti-inflammatory activity of salvianolic acid B in microglia contributes to its neuroprotective effect. Neurochem Res 2010;35:1029–1037.

Luo P, Tan Z, Zhang Z, Li H, Mo Z. Inhibitory effects of salvianolic acid B on the high glucose-induced mesangial proliferation via NF-κB-dependent pathway. Biol Pharm Bull 2008;31:1381–1386.

Xie LX, Durairajan SS, Lu JH, Liu CL, Kum WF, Wang Y, et al. The effect of salvianolic acid B combined with laminar shear stress on TNF-α-stimulated adhesion molecule expression in human aortic endothelial cells. Clin Hemorheol Microcirc 2010;44:245–258.

Maass AH, Buvoli M. Cardiomyocyte preparation, culture, and gene transfer. Methods Mol Biol 2007;366:321–330.

Liu X, Ren Z, Zhan R, Wang X, Wang X, Zhang Z, et al. Prohibitin protects against oxidative stress-induced cell injury in cultured neonatal cardiomyocyte. Cell Stress Chaperones 2009;14:311–319.

de Jong PR, Schadenberg AW, Jansen NJ, Prakken BJ. HSP70 and cardiac surgery: molecular chaperone and inflammatory regulator with compartmentalized effects. Cell Stress Chaperones 2009;14:117–131.

FULL TEXT LINK

More>

浏览量

754

Downloads

CSCD

文章被引用时，请邮件提醒。

Submit

工具集

关联资源

Anti-inflammatory effects of Reduning Injection (热毒宁注射液) on lipopolysaccharide-induced acute lung injury of rats

Berberine inhibits norepinephrine-induced apoptosis in neonatal rat cardiomyocytes via inhibiting ROS-TNF-α-caspase signaling pathway

Effect of safflor yellow injection on inhibiting lipopolysaccharide-induced pulmonary inflammatory injury in mice

Effect of San’ao Decoction (三拗汤) on the airway inflammation and hyperresponsiveness in a murine model of lipopolysaccharide-enhanced asthma

Effect of Jianpi Huoxue decoction (健脾活血方)-containing serum on tumor necrosis factor-α secretion and gene Expression of endotoxin receptors in RAW264.7 cells induced by lipopolysaccharide