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Objective: To explore the molecular mechanism of dexmedetomidine (Dex) protecting ischemia/reperfusion (I/R) myocardium. Methods: Wild type mice were grouped into control (Control) group, sham operation (Sham) group, WT I/R group, WT Dex group, and Dectin-1 knock out mice were grouped into KO I/R group and KO Dex group in the in vivo study (n=6). TTC staining was used to determine the myocardial infarction area (%) of the above six groups of mice. HE staining and pathological analyze was used to determine the myocardial injury. Serum TNF-α, IL-6 and IL-10 levels in mice were detected by ELISA. Flow cytometry (FCM) was used to count and sort of infiltrating M2 macrophages and neutrophils in myocardium. qPCR assay was used to determine the Dectin-1 mRNA expression in the above sorted cells. Results: TTC results showed that there was no myocardial infarction in the mice of Control group and Sham group. Compared with the WT I/R group, the infarct volume was significantly lower in WT Dex group, KO I/R group and KO Dex group (P<0.05) . Compared with the KO I/R group, the infarct volume was reduced in KO Dex group (P< 0.05). The results of HE staining showed that the myocardial fibers of the WT I/R group of mice were disorderly arranged, with a large number of broken myocardial fibers, while the myocardial fibers of the WT Dex group, KO I/R group and KO Dex group of mice had a little breakage, the structural damage was not significant, and the myocardial arrangement was relatively neat. The degree of myocardi中国免疫学杂志 2024 年第 40 卷 al injury of mice in KO Dex group were less than that in KO I/R group mice. ELISA results showed that compared with Sham group, the serum TNF-α and IL-6 levels of the mice in WT I/R group were significantly increased, and the IL-10 level was significantly decreased. Compared with WT I/R group, serum TNF-α and IL-6 levels of the mice in WT Dex group and KO I/R group were significantly decreased, and IL-10 level was significantly increased. Compared with KO I/R group, the serum TNF-α and IL-6 levels of the mice in KO Dex group were significantly decreased, and the IL-10 level was significantly increased (P<0.05). FCM cell counting results showed that compared with Sham group, a large number of M2 macrophages and neutrophils were infiltrated in the myocardium of WT I/R group of mice (P<0.05) . Compared with WT I/R group, the M2 macrophages and neutrophils infiltrated in the myocardium were significantly decreased in WT Dex group, KO I/R group and KO Dex group of mice (P<0.05) . While there was no significant difference between the KO I/R group and the KO Dex group mice (P>0.05) . qPCR results showed that compared with Sham group, the expression level of Dectin-1 mRNA in the myocardial infiltrated M2 macrophages and neutrophils were significantly up-regulated in WT I/ R group of mice (P<0.05) . While compared with WT I/R group, the expression level of Dectin-1 mRNA in Dex group of mice was significantly lower (P<0.05) . Mice in KO I/R group and KO Dex group did not express Dectin-1. Conclusion: The protective mechanisms of Dex preconditioning on I/R injured myocardium involves reducing the infiltrating number of M2 macrophages and neutrophils in myocardium after I/R injury, which may be achieved by inhibiting the expression of Dectin-1. [ABSTRACT FROM AUTHOR]

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Objective To explore the application effect of different doses of dexmedetomidine assisted thoracic paravertebral block (TPVB) in cardiac surgery.Methods A total of 80 patients who underwent off-pump coronary artery bypass grafting (OPCABG) in the hospital from January 2022 to January 2023 were randomly divided into the 0.25 μg/kg dexmedetomidine group (Group A),the 0.50 μg/kg dexmedetomidine group (Group B),the 1.00 μg/kg dexmedetomidine group (Group C) and the placebo group (Group D), with 20 cases in each group. The levels of cortisol (Cor),interleukin-6 (IL-6),visual analogue scale (VAS) score, intensive care unit (ICU) stay time, postoperative mechanical ventilation time, and postoperative hospital stay in each group were compared. Results There were no statistically significant differences in the levels of Cor and IL-6 between the four groups before anesthesia induction and 24 hours after surgery (P＞0.05) .The levels of Cor and IL-6 at 2 hours after the start of surgery, immediately after surgery, and 24 hours after surgery in the four groups were higher than those before anesthesia induction, and the differences were statistically significant (P＜0.05) .The levels of Cor and IL-6 in groups B and Cwere lower than those in groups A and D at 2 hours after the start of surgery and immediately after surgery, and the differences were statistically significant (P＜0.05) .There was statistically significant difference in VAS scores immediately after extubation and 12 hours after surgery among the four groups, with groups B and C having lower VAS scores than groups A and D (P＜0.05) .There was no statistically significant difference in VAS scores at 24 hours after surgery among the four groups (P＞0.05) .There were no statistically significant differences in VAS scores at different time points in each group (P＞0.05) .There were no statistically significant differences in ICU stay time, postoperative mechanical ventilation time, and postoperative hospitalization time among the four groups (P＞0.05) .Conclusion Dexmedetomidine assisted TPVB can inhibit the perioperative stress response of OPCABG, improve the postoperative pain, and 0.50 μg/kg dexmedetomidine is recommended as an adjuvant dose for TPVB. [ABSTRACT FROM AUTHOR]

Objective: To investigate the protective effect of dexmedetomidine (DEX) on myocardial ischemia-reperfusion injury in diabetic mice and its possible molecular mechanism. Methods: Sixty 8-week-old SPF C57BL mice were fed with high fat for 6 weeks. At the 7th week, the type 2 diabetes model was established by intraperitoneal injection of streptozotocin (STZ) 45 mg/kg/d once a day for5 days. After modeling, the mice were randomly divided into sham operation group (sham group), ischemia-reperfusion group (I/R group), hypoxia-inducible factor-1α (HIF-1α) inhibitor 2ME2 group (2ME2 group), DEX group and DEX+2ME2 group (DM group), with 12mice in each group. In sham group, the skin was only cut and sutured. In the other four groups, the left anterior descending coronary artery was ligated through thoracotomy, and the ligating wire was released after 60 minutes of ischemia, followed by 120 minutes of reperfusion to establish the ischemia-reperfusion injury model. Blood samples were collected from the abdominal aorta at 120 min of reperfusion for determination of serum concentrations of troponin I (cTnI), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α)by ELISA. Then the mice were sacrificed and left ventricles were isolated for observation of morphology and structure of myocardium by HE staining. The expression of HIF-1α and NOD-like receptor protein 3 (NLRP3) was detected by Western blot. Cardiac function was assessed by echocardiography at 24 h of reperfusion. Results: Compared with sham group, the concentrations of cTnI, IL-1β and TNF-α were significantly increased, myocardial tissue structure disorder, myocardial fiber rupture, myocardial cell swelling, inflammatory cell infiltration were significantly increased, the expression of NLRP3 in myocardial tissue was significantly increased, and stroke volume (SV), ejection fraction (EF) % and fractional shortening (FS) % were significantly decreased in I/R, 2ME2, DEX and DM groups (P＜0.05).Compared with I/R group, the expression of HIF-1α was significantly increased, the expression of NLRP3 was significantly decreased, the concentrations of cTnI, IL-1β and TNF-α were significantly decreased, myocardial tissue structure was significantly improved, inflammatory cell infiltration was significantly decreased, SV, EF and FS were significantly increased in DEX and DM groups (P＜0.05). Compared with the DEX group, the expression of HIF-1α was significantly decreased, the expression of NLRP3 was significantly increased, the concentrations of cTnI, IL-1β and TNF-α were significantly increased, myocardial tissue structure disorder, myocardial fiber rupture, myocardial cell swelling, inflammatory cell infiltration were significantly increased, SV, EF and FS were significantly decreased in the DM group (P＜0.05). Conclusions: DEX can alleviate myocardial I/R injury in diabetic mice by up-regulating HIF-1α, inhibiting the activation of NLRP3 inflammasome and reducing inflammatory response. [ABSTRACT FROM AUTHOR]

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Copyright of Engineering Management & Technology Discussion is the property of Omniscient Pte. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Diabetes Mellitus is the property of Chinese Journal of Diabetes Mellitus and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)