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Baicalein retards proliferation and collagen deposition by activating p38MAPK-JNK via microRNA-29

Xiaoliang Yang1, Chunyan Zhang2, Jinjie Jiang1

  • 1Department of Burn and Plastic Surgery, Qingdao Central Hospital (The Affiliated Central Hospital of Qingdao University), Qingdao, China.

Journal of Cellular Biochemistry
|May 14, 2019
PubMed

Insights

Baicalein (BAI) inhibits scar formation by upregulating microRNA-29 (miR-29), reducing collagen deposition and cell proliferation. BAI activates the p38MAPK/JNK pathway, a mechanism dependent on miR-29.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Dermatology

Background:

  • Excessive collagen deposition causes hypertrophic scars and keloids.
  • MicroRNA-29 (miR-29) is a key regulator in scar formation.
  • Baicalein (BAI) is known to impair scar formation, but its mechanism involving miR-29 is unclear.

Purpose of the Study:

  • To investigate the role of miR-29 in baicalein's (BAI) antifibrotic effects.
  • To elucidate the molecular mechanism by which BAI inhibits scar formation.
  • To determine if BAI-mediated inhibition of collagen synthesis involves the p38MAPK/JNK pathway.

Main Methods:

  • NIH-3T3 cells were treated with BAI and/or TGF-β1.
  • Cell viability was assessed using CCK-8 and Western blot.
  • Collagen synthesis (total soluble collagen, collagen 1, α-SMA) was measured via Sircol assay and qRT-PCR/Western blot.
  • miR-29 inhibitor transfection was performed and verified by qRT-PCR.
  • Phosphorylated p38MAPK and JNK levels were analyzed by Western blot.

Main Results:

  • BAI reduced NIH-3T3 cell proliferation and TGF-β1-induced collagen synthesis (collagen 1, α-SMA) at mRNA and protein levels.
  • Upregulation of miR-29 by BAI was confirmed.
  • Inhibition of miR-29 reversed the antifibrotic effects of BAI.
  • BAI promoted the phosphorylation of p38MAPK and JNK, which was reversed by the miR-29 inhibitor.

Conclusions:

  • Baicalein (BAI) inhibits cell proliferation and collagen deposition, key factors in scar formation.
  • BAI exerts its antifibrotic effects by upregulating miR-29.
  • BAI activates the p38MAPK/JNK signaling pathway through miR-29 upregulation, offering a potential therapeutic mechanism for scar reduction.
Keywords:
baicaleincollagenmicroRNA-29proliferation

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