Korean J Pain.  2021 Jan;34(1):19-26. 10.3344/kjp.2021.34.1.19.

The proper concentrations of dextrose and lidocaine in regenerative injection therapy: in vitro study

Affiliations
  • 1Department of Convergence Medical Science, Gyeongsang National University, Jinju, Korea
  • 2Department of Anesthesiology and Pain Medicine, Gyeongsang National University Changwon Hospital, Changwon, Korea
  • 3Department of Anesthesiology and Pain Medicine, Gyeongsang National University Hospital, Jinju, Korea
  • 4Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju, Korea
  • 5Department of Anesthesiology and Pain Medicine, Gyeongsang National University College of Medicine, Jinju, Korea

Abstract

Background
Prolotherapy is a proliferation therapy as an alternative medicine. A combination of dextrose solution and lidocaine is usually used in prolotherapy. The concentrations of dextrose and lidocaine used in the clinical field are very high (dextrose 10%-25%, lidocaine 0.075%-1%). Several studies show about 1% dextrose and more than 0.2% lidocaine induced cell death in various cell types. We investigated the effects of low concentrations of dextrose and lidocaine in fibroblasts and suggest the optimal range of concentrations of dextrose and lidocaine in prolotherapy.
Methods
Various concentrations of dextrose and lidocaine were treated in NIH-3T3. Viability was examined with trypan blue exclusion assay and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Migration assay was performed for measuring the motile activity. Extracellular signal-regulated kinase (Erk) activation and protein expression of collagen I and α-smooth muscle actin (α-SMA) were determined with western blot analysis.
Results
The cell viability was decreased in concentrations of more than 5% dextrose and 0.1% lidocaine. However, in the concentrations 1% dextrose (D1) and 0.01% lidocaine (L0.01), fibroblasts proliferated mildly. The ability of migration in fibroblast was increased in the D1, L0.01, and D1 + L0.01 groups sequentially. D1 and L0.01 increased Erk activation and the expression of collagen I and α-SMA and D1 + L0.01 further increased. The inhibition of Erk activation suppressed fibroblast proliferation and the synthesis of collagen I.
Conclusions
D1, L0.01, and the combination of D1 and L0.01 induced fibroblast proliferation and increased collagen I synthesis via Erk activation.

Keyword

Actins; Cell Migration Assay; Cell Proliferation; Collagen Type 1; Extracellular Signal-Regulated MAP Kinases; Fibroblast; Glucose; Lidocaine; Muscle; Smooth; Prolotherapy
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