Search

Colistin is an effective antibiotic against multidrug-resistant gram-negative bacterial infections; however, neurotoxic effects are fundamental dose-limiting factors for this treatment. Stem cell therapy is a promising method for treating neuronal diseases. Multipotent mesenchymal stromal cells (MSC) represent a promising source for regenerative medicine. Identification of neuroprotective agents that can be co-administered with colistin has the potential to allow the clinical application of this essential drug. This study was conducted to assess the potential protective effects of MSC, against colistin-induced neurotoxicity, and the possible mechanisms underlying any effect. Forty adult female albino rats were randomly classified into four equal groups; the control group, the MSC-treated group (A single dose of 1 × 106/mL MSCs through the tail vein), the colistin-treated group (36 mg/kg/d colistin was given for 7 d) and the colistin and MSC treated group (36 mg/kg/d colistin was administered for 7 d, and 1 × 106/mL MSCs). Colistin administration significantly increased GFAP, NGF, Beclin-1, IL-6, and TNF-α immunreactivity intensity. MSC administration in colistin-treated rats partially restored each of these markers. Histopathological changes in brain tissues were also alleviated by MSC co-treatment. Our study reveals a critical role of inflammation, autophagy, and apoptosis in colistin-induced neurotoxicity and showed that they were markedly ameliorated by MSC co-administration. Therefore, MSC could represent a promising agent for prevention of colistin-induced neurotoxicity. [ABSTRACT FROM AUTHOR]

Background/aim: In this study, we aimed to compare the effects of propofol-ketamine and propofol-fentanyl sedations on postprocedure nausea-vomiting in children undergoing magnetic resonance imaging (MRI). Materials and methods: This study included 100 pediatric patients (2–10 years old) who had propofol-ketamine and propofol-fentanyl for sedation to undergo MRI. The patients were divided into two groups, and sedation was performed through propofol-ketamine (Group K; n = 50) or propofol-fentanyl (Group F; n = 50). For sedation induction, intravenous (IV) bolus of 1.2 mg/kg propofol and 1 mg/kg ketamine were administered in Group K, IV bolus of 1.2 mg/kg propofol, and 1 µg/kg fentanyl in Group F. All patients received 0.5 mg/kg IV bolus propofol in additional doses when the Ramsay Sedation Score (RSS) was below 4 for maintenance. Perioperative heart rate, systolic arterial pressure, peripheral oxygen saturation, respiratory rate, and nausea-vomiting scores were recorded for each patient. Results: There was no difference between the groups in terms of nausea incidences at the 1st hour. However, the rate of vomiting was significantly higher in Group K. Conclusion: In our study, we showed that the vomiting rate was higher in the 1st hour in Group K compared to Group F. [ABSTRACT FROM AUTHOR]

Objective: Cisplatin (CDDP) has been known to be an effective antineoplastic drug; however, it has a cardiotoxic effect. Curcumin (CMN) and beta-carotene (BC) have been suggested to protect biological systems against CDDP-induced damage. The current study was conducted to evaluate the possible protective roles of CMN and BC on CDDP-induced cardiotoxicity in rat cardiac tissues., Methods: A total of 49 adult female Wistar albino rats were equally divided into seven groups as follows: control (no medication), sesame oil (1 mg/kg), CDDP (single dose injection two times as once a week, 5 mg/kg/week), BC (100 mg/kg), CDDP+BC (pretreated BC for 30 min before CDDP injection), CMN (200 mg/kg), and CDDP+CMN (pretreated CMN for 30 min before CDDP injection). These treatments were applied intraperitoneally for CDDP and with gavage for CMN and BC. The oxidative/antioxidant indicators, inflammatory cytokines, and histopathological alterations were examined., Results: These alterations included a marked increase in malondialdehyde (MDA) level, significant decrease in catalase (CAT) and superoxide dismutase (SOD) activities, and significant elevation of tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, interleukin (IL)-6 in the CDDP group compared with the other groups. Histopathologically, CDDP-induced severe myocardial degenerative changes were observed. However, the CDDP-induced disturbances in the above-mentioned parameters significantly improved by treatment with BC and particularly CMN., Conclusion: This study indicated that CDDP treatment markedly caused cardiotoxicity; however, treatment with CMN or BC ameliorated this cardiotoxicity in rats. Furthermore, these findings revealed that treatment with CMN has a higher cardioprotective effect than that with BC against CDDP-induced cardiotoxicity in rat cardiac tissues.