Systemic lidocaine inhibits high-mobility group box 1 messenger ribonucleic acid expression and protein in BALB/c mice after closed fracture musculoskeletal injury

Robert Hotman Sirait; Mochammad Hatta; Muhammad Ramli; Andi Asadul Islam; Syafrie Kamsul Arief

doi:10.4103/sja.SJA_685_17

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ORIGINAL ARTICLE

Year : 2018 | Volume : 12 | Issue : 3 | Page : 395-398

Systemic lidocaine inhibits high-mobility group box 1 messenger ribonucleic acid expression and protein in BALB/c mice after closed fracture musculoskeletal injury

Robert Hotman Sirait¹, Mochammad Hatta², Muhammad Ramli³, Andi Asadul Islam⁴, Syafrie Kamsul Arief³
¹ Department of Anesthesiology, Faculty of Medicine, Christian University of Indonesia, Jakarta; Department of Microbiology, Molecular Biology and Immunology Laboratory, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia
² Department of Microbiology, Molecular Biology and Immunology Laboratory, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia
³ Department of Anesthesiology, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia
⁴ Department of Neurosurgery, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia

Correspondence Address:
Prof. Mochammad Hatta
Molecular Biology and Immunology Laboratory, Faculty of Medicine, Hasanuddin University, Makassar
Indonesia

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/sja.SJA_685_17

Background: Severe musculoskeletal trauma can trigger an inflammatory response, and an excessive inflammatory response can lead to systemic inflammatory response syndrome and multiorgan failure. High-mobility group box 1 (HMGB1) is an early mediator pro-inflammatory cytokine in sterile injuries and a late cytokine mediator in infection and sepsis. Previous research has shown that administration of systemic lidocaine can inhibit HMGB1 expression in macrophages of septic rats. The aim of this study was to demonstrate the efficacy of systemic lidocaine to inhibit HMGB1 mRNA and protein in a BALB/c mouse model of sterile inflammation due to closed fracture musculoskeletal injury. Materials and Methods: Twenty adult male BALB/c mice were divided into lidocaine and control groups. The closed fracture musculoskeletal injury was performed by breaking the left thigh bone of the mice. Four hours after undergoing the closed fracture, the lidocaine group was treated with lidocaine intravenous (2 mg/kg). The same volume of distilled water was injected into the control group instead of lidocaine. HMGB1 mRNA expression was examined with real-time polymerase chain reaction, and HMGB1 protein level was determined with enzyme-linked immunosorbent assay. Results: The expression of HMGB1 mRNA and protein levels in mice that sustained inflammation due to a closed fracture musculoskeletal injury was significantly decreased in the lidocaine group (P < 0.00 and P < 0.00 for mRNA and protein, respectively). Conclusions: Intravenous administration of lidocaine effectively inhibited the inflammatory process in BALB/c mice that underwent closed fracture musculoskeletal injury by suppressing HMGB1 mRNA transcription and HMGB1 protein translation.

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