Experimental and therapeutic medicine最新文献

[This retracts the article DOI: 10.3892/etm.2019.7316.].

Intracranial infection is a complication of neurosurgery that can lead to severe neurological complications, greatly increasing the risk of mortality. Intracranial infection caused by multidrug-resistant Acinetobacter baumannii (MDR-AB) is one of the most severe complications of craniotomy. However, the availability of effective therapeutic options for such infections remains limited. Therefore, the present study aimed to assess the therapeutic efficacy of intrathecal/intracerebral (ITC) ventricle tigecycline injection for managing post-neurosurgical intracranial infections caused by MDR-AB. The present retrospective study was conducted from January 2014 to December 2023 at the Second Affiliated Hospital of Shandong First Medical University (Taian, China), which included 15 cases of MDR-AB positivity in the cerebrospinal fluid (CSF) cultures after neurosurgery. Patients treated with intravenous and intrathecal/ITC tigecycline ventricle injection were assigned to the 'ITV + ITC' group, whereas patients treated without intrathecal/ITC injection were assigned to the 'ITV' group. Data for general information, treatment history, the results of biochemical indicators in CSF and the microbiological clearance rate were collected and analyzed. No significant differences were observed in characteristics, susceptibility testing or empirical antimicrobial use between the two groups after treatment. However, after treatment, the ITV + ITC group exhibited a significantly decreased body temperature, whilst the biochemical indicators present in CSF were significantly improved. In addition, the ITV + ITC group had a significantly higher microbiological clearance rate (5/6; 83.33%) compared with that in the ITV group (2/9; 22.22%). These findings suggest that intravenous plus intrathecal/ITC ventricle injection of tigecycline is an effective regimen for treating intracranial infections caused by MDR-AB.

The therapeutic role of blockade of cysteinyl leukotriene receptor 1 (CysLTR1) in asthma has been previously studied. However, the effect of CysLTR1 blockade on bronchial epithelial cell apoptosis and the nuclear factor erythroid-derived 2-related factor 2 (Nrf2) signaling pathway remains unclear. The present study established an ovalbumin (OVA)-induced asthmatic rat model. Varying doses (1, 4 and 30 mg/kg) of montelukast sodium, a specific CysLTR1 antagonist, were used to inhibit CysLTR1 function in an asthmatic rat model. Reverse transcription-quantitative PCR was used to detect the expression levels of CysLTR1, NAD(P)H quinone oxidoreductase 1 (NQO1) and heme oxygenase 1 (HO-1). CysLTR1 and Nrf2 protein expression levels were determined using western blotting. Immunofluorescence assays were used to evaluate the relative fluorescence intensity of Nrf2 in rat lung tissues. Lung tissue histology was assessed through hematoxylin & eosin, alcian blue and periodic acid-Schiff and Masson's trichrome staining assays. The levels of IL-17, IL-4, serum IgE and the reduced/oxidized glutathione ratio were determined using ELISA assay kits. The number of inflammatory cells was analyzed using Wright-Giemsa staining. Bronchial epithelial cell apoptosis was measured using a TUNEL assay. The results indicated that OVA-induced inflammatory responses and increased eosinophil, lymphocyte and macrophage counts were significantly attenuated following blockade of CysLTR1. Downregulated expression of antioxidant genes NQO1 and HO-1 and the reduced GSH/GSSG ratio caused by OVA challenge were restored by blockade of CysLTR1. Additionally, CysLTR1 blockade also reduced collagen deposition, suppressed goblet cell hyperplasia and inhibited bronchial epithelial cell apoptosis in a rat model of asthma. Furthermore, it was demonstrated that the blockade of CysLTR1 could significantly increase Nrf2 expression. In conclusion, the blockade of CysLTR1 could alleviate asthma in an OVA-induced rat model by inhibiting bronchial epithelial cell apoptosis and activating the Nrf2 signaling pathway. These data may potentially provide a theoretical basis for future asthma therapy in a clinical setting.