2. Academic Validation
  3. Liquiritin reduces lipopolysaccharide-aroused HaCaT cell inflammation damage via regulation of microRNA-31/MyD88

Liquiritin reduces lipopolysaccharide-aroused HaCaT cell inflammation damage via regulation of microRNA-31/MyD88

  • Int Immunopharmacol. 2021 Dec;101(Pt B):108283. doi: 10.1016/j.intimp.2021.108283.
Xuehui Yang 1,  Xiuwei Dang 2,  Xue Zhang 3,  Siren Zhao 4
Affiliations

Affiliations

  • 1 Nursing Department, Shandong Provincial Third Hospital, Jinan, Shandong 250031, China.
  • 2 Department of Medicine and Chemical Engineering, Jinan Technician College, Jinan, Shandong 250031, China.
  • 3 Department of Operating Room, Tianqiao People's Hospital of Jinan, Jinan, Shandong 250031, China.
  • 4 Department of Neurosurgery, Shandong Provincial Third Hospital, Jinan, Shandong 250031, China. Electronic address: [email protected].
PMID: 34731782 DOI: 10.1016/j.intimp.2021.108283
Abstract

Background: Pressure ulcers are a common issue for people who have limited mobility. This study tested the impact of liquiritin on human keratinocyte HaCaT cell inflammatory damage aroused by lipopolysaccharide (LPS).

Methods: HaCaT cells were underwent LPS and/or liquiritin incubation. Cell viability, Apoptosis and inflammatory molecules interleukin 6 (IL-6), tumor necrosis factor α (TNF-α) and cyclooxygenase-2 (COX-2) expressions, along with nuclear factor kappa B (NF-κB) and c-Jun N-terminal kinase (JNK) pathways activities were tested by MTT assay, Guava Nexin assay, ELISA and western blotting, respectively. qRT-PCR was done for measuring microRNA-31 (miR-31) expression. miR-31 inhibitor was transfected to silence miR-31. Animal pressure ulcers was established on the dorsal skin of adult rats. The effects of liquiritin on wound healing were analyzed by measuring wound closure rates.

Results: LPS aroused HaCaT cell inflammatory damage, as evidenced by the decrease of cell viability, increase of cell Apoptosis and enhanced expressions of IL-6, TNF-α and COX-2. Liquiritin protected HaCaT cells against LPS-aroused inflammatory damage through increasing cell viability, decreasing cell Apoptosis, and reducing IL-6, TNF-α and COX-2 expressions. Liquiritin attenuated the LPS-aroused NF-κB and JNK pathways activation in HaCaT cells. Rat pressure ulcers model also confirmed that liquiritin promoted wound healing. In mechanism, miR-31 expression was boosted by liquiritin in HaCaT cells. Silencing miR-31 weakened the impacts of liquiritin on LPS-irritated HaCaT cells. Myeloid differentiation factor 88 (MyD88) was a target of miR-31 in HaCaT cells.

Conclusion: This research affirmed the beneficial impact of liquiritin on pressure ulcers. Liquiritin reduced LPS-aroused HaCaT cell inflammatory damage might be implemented via raising miR-31 expression, lowering MyD88 expression, and repressing NF-κB and JNK pathways.

Keywords

JNK pathway; Liquiritin; MicroRNA-31; MyD88; NF-κB pathway; Pressure ulcers.

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