Protective mechanisms of resveratrol derivatives against TNF-α-induced inflammatory responses in rat mesangial cells

I-Ta Lee, Chwan Fwu Lin, Yu Ling Huang, Kowit Yu Chong, Ming Fa Hsieh, Tse Hung Huang, Ching Yi Cheng

Research output: Contribution to journalArticle

Abstract

Introduction: Resveratrol has been reported to alleviate inflammatory responses and oxidative stress in mesangial cells and in several types of renal injury in animal models. Previously, the active resveratrol derivatives from the roots of Vitis thunbergii Sieb. & Zucc. (Vitaceae) were shown to have significant anti-platelet and anti-oxidative activities. However, the anti-inflammatory mechanisms of these resveratrol derivatives in rat mesangial cells (RMCs) have not been clarified fully. Methods: The protective mechanisms of resveratrol derivatives involved in tumor necrosis factor-α (TNF-α)-induced inflammatory responses were assessed by Western blot analysis, real-time PCR, and RT–PCR. The involvement of various signaling molecules in these responses was investigated using selective pharmacological inhibitors. Results: Nontoxic concentrations of the resveratrol derivatives significantly attenuated cytosolic phospholipase A2 (cPLA2) and cyclooxygenase 2 (COX-2) expression in RMCs challenged by TNF-α. These resveratrol derivatives inhibited TNF-α-activated ERK1/2 and JNK1/2 without affecting p38 phosphorylation. Next, we demonstrated that TNF-α induced NF-κB activation, translocation, and promoter activity, which was inhibited by pretreatment with resveratrol derivatives in RMCs. Conclusion: The protective mechanisms of resveratrol derivatives against TNF-α-stimulated inflammatory responses via cPLA2/COX-2/PGE2 inhibition was caused by the attenuation of the JNK1/2, ERK1/2, and NF-κB signaling pathways in RMCs.

Original languageEnglish
Pages (from-to)380-392
Number of pages13
JournalCytokine
Volume113
DOIs
Publication statusPublished - Jan 1 2019
Externally publishedYes

Fingerprint

Mesangial Cells
Rats
Tumor Necrosis Factor-alpha
Derivatives
Cytosolic Phospholipases A2
Cyclooxygenase 2
Vitaceae
Phosphorylation
Oxidative stress
resveratrol
Vitis
Platelets
Dinoprostone
Real-Time Polymerase Chain Reaction
Animals
Oxidative Stress
Anti-Inflammatory Agents
Blood Platelets
Animal Models
Western Blotting

Keywords

  • Cyclooxygenase 2
  • Cytokine
  • Inflammation
  • Mesangial cells
  • Resveratrol derivatives

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Biochemistry
  • Hematology
  • Molecular Biology

Cite this

Protective mechanisms of resveratrol derivatives against TNF-α-induced inflammatory responses in rat mesangial cells. / Lee, I-Ta; Lin, Chwan Fwu; Huang, Yu Ling; Chong, Kowit Yu; Hsieh, Ming Fa; Huang, Tse Hung; Cheng, Ching Yi.

In: Cytokine, Vol. 113, 01.01.2019, p. 380-392.

Research output: Contribution to journalArticle

Lee, I-Ta ; Lin, Chwan Fwu ; Huang, Yu Ling ; Chong, Kowit Yu ; Hsieh, Ming Fa ; Huang, Tse Hung ; Cheng, Ching Yi. / Protective mechanisms of resveratrol derivatives against TNF-α-induced inflammatory responses in rat mesangial cells. In: Cytokine. 2019 ; Vol. 113. pp. 380-392.
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AU - Hsieh, Ming Fa

AU - Huang, Tse Hung

AU - Cheng, Ching Yi

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N2 - Introduction: Resveratrol has been reported to alleviate inflammatory responses and oxidative stress in mesangial cells and in several types of renal injury in animal models. Previously, the active resveratrol derivatives from the roots of Vitis thunbergii Sieb. & Zucc. (Vitaceae) were shown to have significant anti-platelet and anti-oxidative activities. However, the anti-inflammatory mechanisms of these resveratrol derivatives in rat mesangial cells (RMCs) have not been clarified fully. Methods: The protective mechanisms of resveratrol derivatives involved in tumor necrosis factor-α (TNF-α)-induced inflammatory responses were assessed by Western blot analysis, real-time PCR, and RT–PCR. The involvement of various signaling molecules in these responses was investigated using selective pharmacological inhibitors. Results: Nontoxic concentrations of the resveratrol derivatives significantly attenuated cytosolic phospholipase A2 (cPLA2) and cyclooxygenase 2 (COX-2) expression in RMCs challenged by TNF-α. These resveratrol derivatives inhibited TNF-α-activated ERK1/2 and JNK1/2 without affecting p38 phosphorylation. Next, we demonstrated that TNF-α induced NF-κB activation, translocation, and promoter activity, which was inhibited by pretreatment with resveratrol derivatives in RMCs. Conclusion: The protective mechanisms of resveratrol derivatives against TNF-α-stimulated inflammatory responses via cPLA2/COX-2/PGE2 inhibition was caused by the attenuation of the JNK1/2, ERK1/2, and NF-κB signaling pathways in RMCs.

AB - Introduction: Resveratrol has been reported to alleviate inflammatory responses and oxidative stress in mesangial cells and in several types of renal injury in animal models. Previously, the active resveratrol derivatives from the roots of Vitis thunbergii Sieb. & Zucc. (Vitaceae) were shown to have significant anti-platelet and anti-oxidative activities. However, the anti-inflammatory mechanisms of these resveratrol derivatives in rat mesangial cells (RMCs) have not been clarified fully. Methods: The protective mechanisms of resveratrol derivatives involved in tumor necrosis factor-α (TNF-α)-induced inflammatory responses were assessed by Western blot analysis, real-time PCR, and RT–PCR. The involvement of various signaling molecules in these responses was investigated using selective pharmacological inhibitors. Results: Nontoxic concentrations of the resveratrol derivatives significantly attenuated cytosolic phospholipase A2 (cPLA2) and cyclooxygenase 2 (COX-2) expression in RMCs challenged by TNF-α. These resveratrol derivatives inhibited TNF-α-activated ERK1/2 and JNK1/2 without affecting p38 phosphorylation. Next, we demonstrated that TNF-α induced NF-κB activation, translocation, and promoter activity, which was inhibited by pretreatment with resveratrol derivatives in RMCs. Conclusion: The protective mechanisms of resveratrol derivatives against TNF-α-stimulated inflammatory responses via cPLA2/COX-2/PGE2 inhibition was caused by the attenuation of the JNK1/2, ERK1/2, and NF-κB signaling pathways in RMCs.

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