The proper concentrations of dextrose and lidocaine in regenerative injection therapy: in vitro study
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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.
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.
참고문헌 (27)
- Banks AR, "A rationale for prolotherapy", J Orthop Med, 13, pp.54~59 (1991)
- Reeves KD, "Pain procedures in clinical practice", pp.172~190 (2000), Hanley & Belfus
- Sung CM, "Cytotoxic effects of ropivacaine, bupivacaine, and lidocaine on rotator cuff tenofibroblasts", Am J Sports Med, 42, pp.2888~2896 (2014)
- Rabago D, "Prolotherapy in primary care practice", Prim Care, 37, pp.65~80 (2010)
- Reeves KD, "Long-term effects of dextrose prolotherapy for anterior cruciate ligament laxity", Altern Ther Health Med, 9, pp.58~62 (2003)
- Topol GA, "Efficacy of dextrose prolotherapy in elite male kicking-sport athletes with chronic groin pain", Arch Phys Med Rehabil, 86, pp.697~702 (2005)
- Lyftogt J, "Subcutaneous prolotherapy treatment of refractory knee, shoulder, and lateral elbow pain", Australas Musculoskelet Med, 12, pp.110~112 (2007)
- Wang D, "Transcription factor Egr1 is involved in high glucose-induced proliferation and fibrosis in rat glomerular mesangial cells", Cell Physiol Biochem, 36, pp.2093~2107 (2015)
- Shin ES, "High glucose alters retinal astrocytes phenotype through increased production of inflammatory cytokines and oxidative stress", PLoS One, 9, pp.e103148~ (2014)
- Shi L, "Liraglutide attenuates high glucose-induced abnormal cell migration, proliferation, and apoptosis of vascular smooth muscle cells by activating the GLP-1 receptor, and inhibiting ERK1", 2 and PI3K, Cardiovasc Diabetol, pp.2015, 14[DOI]
- Han J, "Glucose promotes cell proliferation, glucose uptake and invasion in endometrial cancer cells via AMPK", mTOR, Gynecol Oncol, pp.2015, 138[DOI]
- Saengboonmee C, "High glucose enhances progression of cholangiocarcinoma cells via STAT3 activation", Sci Rep, 6, pp.18995~ (2016)
- Wang R, "Effect of glucagon-like peptide-1 on high-glucose-induced oxidative stress and cell apoptosis in human endothelial cells and its underlying mechanism", J Cardiovasc Pharmacol, 66, pp.135~140 (2015)
- Tsai HY, "Coenzyme Q10 attenuates high glucose-induced endothelial progenitor cell dysfunction through AMP-activated protein kinase pathways", J Diabetes Res, 2016, pp.6384759~ (2016)
- Cheng NC, "High glucoseinduced reactive oxygen species generation promotes stemness in human adipose-derived stem cells", Cytotherapy, 18, pp.371~383 (2016)
- Qu L, "Quercetin alleviates high glucose-induced Schwann cell damage by autophagy", Neural Regen Res, 9, pp.1195~1203 (2014)
- Lee HT, "Local anesthetics induce human renal cell apoptosis", Am J Nephrol, 23, pp.129~139 (2003)
- Kamiya Y, "Lidocaine-induced apoptosis and necrosis in U937 cells depending on its dosage", Biomed Res, 26, pp.231~239 (2005)
- Grishko V, "Apoptosis and mitochondrial dysfunction in human chondrocytes following exposure to lidocaine, bupivacaine, and ropivacaine", J Bone Joint Surg Am, 92, pp.609~618 (2010)
- Chang YC, "Local anesthetics induce apoptosis in human thyroid cancer cells through the mitogen-activated protein kinase pathway", PLoS One, 9, pp.e89563~ (2014)
- Chang YC, "Local anesthetics induce apoptosis in human breast tumor cells", Anesth Analg, 118, pp.116~124 (2014)
- Onizuka S, "Clinical dose of lidocaine destroys the cell membrane and induces both necrosis and apoptosis in an identified Lymnaea neuron", J Anesth, 26, pp.54~61 (2012)
- Zhang W, "MAPK signal pathways in the regulation of cell proliferation in mammalian cells", Cell Res, 12, pp.9~18 (2002)
- Sugimoto R, "High glucose stimulates hepatic stellate cells to proliferate and to produce collagen through free radical pro-duction and activation of mitogen-activated protein kinase", Liver Int, 25, pp.1018~1026 (2005)
- Tang M, "High glucose promotes the production of collagen types I and III by cardiac fibroblasts through a pathway dependent on extracellular-signal-regulated kinase 1", 2, 2007, pp.301, 109~114
- Darby IA, "Fibroblasts and myofibroblasts in wound healing", Clin Cosmet Investig Dermatol, 7, pp.301~311 (2014)
- Zhang C, "ERK2small interfering RNAs prevent epidural fibrosis via the efficient inhibition of collagen expression and inflammation in laminectomy rats", Biochem Biophys Res Commun, 444, pp.395~400 (2014)