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BACKGROUND: The objective of the present study was to evaluate the effect of dexmedetomidine administration during video-assisted thoracoscopic surgery for lung cancer on perioperative inflammatory response and chronic post-surgical pain. METHODS: A cohort of 152 patients with lung cancer scheduled for elective video-assisted thoracoscopic surgery participated in this randomized controlled trial. Patients were randomly divided into 2 groups and administered an equivalent volume of dexmedetomidine (n = 63) or normal saline (n = 63). Dexmedetomidine was administered at a dose of 0.6 µg/kg 10 minutes before anesthesia induction and maintained at 0.5 µg/kg/h until 0.5 hours before surgery completed. Anesthesia and postoperative pain management protocols were standardized for both groups. The analysis included vital signs, numerical rating scales of pain, blood inflammatory and oxidative stress biomarkers, pain type and location, patient-controlled intravenous analgesia usage, consumption of general anesthetics and pain rescue medications, as well as complications. RESULTS: The administration of dexmedetomidine resulted in decreased levels of inflammatory cytokines (interleukin-1 beta, interleukin-6, alongside tumor necrosis factor-alpha) and oxidative stress biomarkers (reactive oxygen species alongside malondialdehyde) but elevated levels of interleukin-10 and superoxide dismutase. In addition, the dexmedetomidine group showed lower postoperative numerical rating scale scores, reduced consumption of anesthetics, faster chest-tube removal, fewer patient-controlled intravenous analgesia presses, and shorter postoperative hospital stays. CONCLUSION: The administration of dexmedetomidine effectively attenuated surgical inflammation, oxidative stress, and postoperative pain, thereby promoting patient recovery after lung cancer surgery without increasing the risk of adverse effects or complications.
RESUMO
OBJECTIVE: Emperipolesis is a pathological feature for the diagnosis of autoimmune hepatitis (AIH). We have previously found that CD8+ T cells participated in the emperipolesis in AIH. In this study we aimed to clarify the characteristics and molecular mechanisms of emperipolesis in patients with AIH in vitro and in mice with α-Galactosylceramide (α-GalCer)-induced acute hepatitis. METHODS: The peripheral blood mononuclear cells (PBMC) of patients with various chronic liver diseases and healthy controls were co-cultured with hepatic cell lines to induce emperipolesis in vitro. Confocal staining was performed to illustrate the cellular types and potential mechanisms of emperipolesis in AIH. In addition, a murine model of α-GalCer-induced acute hepatitis that mimics human AIH was used to confirm the role of CD44/p-ERM/F-actin in the emperipolesis process in vivo. RESULTS: In the co-cultured system of PBMC and hepatic cell line, emperipolesis was observed most commonly in patients with AIH. The main cells participating in emperipolesis were CD8+ T cells, and they penetrated hepatic cells actively via the CD44/p-ERM/F-actin pathway. As a result, most CD8+ T cells engulfed by hepatic cells underwent apoptosis. In the α-GalCer-induced acute hepatitis model, emperipolesis was observed around the inflammatory foci and was inhibited by the ezrin phosphorylation inhibitor NSC668394. Similarly, activated murine CD8+ T cells penetrated primary hepatocytes via the CD44/p-ERM/F-actin pathway in vitro. CONCLUSIONS: CD8+ T cells penetrate hepatic cells actively via the CD44/p-ERM/F-actin signaling pathway and undergo apoptosis. This may be a compensatory mechanism to attenuate the overwhelming immune attack in AIH.