At P35, the learning and memory abilities were assessed in each mouse using a Morris water maze test. Dexmedetomidine significantly decreased the expression of activated caspase‑3 following sevoflurane exposure. Moreover, dexmedetomidine significantly decreased the levels of TNF‑α, IL‑1β and IL‑6 in the hippocampus. SOD activity also increased in a dose‑dependent manner in dexmedetomidine‑treated mice. MDA decreased in a dose‑dependent manner in dexmedetomidine‑treated mice. Lastly, sevoflurane‑induced learning and memory impairment was reversed by dexmedetomidine treatment. By contrast, co‑administration of yohimbine significantly attenuated the neuroprotective effects of dexmedetomidine. These findings suggested that dexmedetomidine exerted a neuroprotective effect against sevoflurane‑induced apoptosis, inflammation, oxidative stress and neurocognitive impairment, which was mediated, at least in part, by α2 adrenoceptors.Acute myocardial infarction (AMI) is a common cardiac disease. Long non‑coding RNA maternally expressed 3 (MEG3) is associated with cellular processes in numerous complicated diseases, including AMI. However, the mechanism underlying MEG3 in myocardial hypoxia is not completely understood. The present study aimed to investigate the underlying mechanism of MEG3 in myocardial hypoxia. The expression levels of hypoxia‑inducible factor 1α (HIF1α), MEG3, microRNA (miR)‑325‑3p, and transient receptor potential cation channel subfamily V member 4 (TRPV4) in hypoxia‑treated H9c2 cells were detected via reverse transcription‑quantitative PCR. The protein expression levels of HIF1α, Bcl‑2, Bax, cleaved caspase‑3 and TRPV4 were detected via western blotting. Cell viability and apoptosis were assessed by performing an MTT assay and flow cytometry, respectively. Lactate dehydrogenase (LDH) release was monitored by conducting an LDH determination assay. The dual‑luciferase reporter assay was performed to verify the targeted relationship between miR‑325‑3p and MEG3 or TRPV4. The expression levels of MEG3 and TRPV4 were significantly increased, whereas miR‑325‑3p expression levels were significantly decreased in hypoxic H9c2 cells compared with normoxic H9c2 cells. In addition, miR‑325‑3p was downregulated by MEG3 compared with the vector group, and miR‑325‑3p targeted TRPV4 in hypoxia‑treated H9c2 cells. The results indicated that MEG3 knockdown attenuated hypoxia‑stimulated injury in H9c2 cells by regulating miR‑325‑3p. TRPV4 knockdown also mitigated hypoxia‑induced injury in H9c2 cells via miR‑325‑3p. Furthermore, compared with the vector group, MEG3 increased TRPV4 expression in hypoxia‑treated H9c2 cells by sponging miR‑325‑3p. Collectively, the results of the present study suggested that MEG3 modulated TRPV4 expression to aggravate hypoxia‑induced injury in rat cardiomyocytes by sponging miR‑325‑3p.Lipid accumulation in podocytes can lead to the destruction of cellular morphology, in addition to cell dysfunction and apoptosis, which is a key factor in the progression of chronic kidney disease (CKD). Berberine (BBR) is an isoquinoline alkaloid extracted from medicinal plants such as model. Cell death was measured using the Cell Counting Kit‑8 colorimetric assay. Cell apoptotic rate was assessed by flow cytometry. The expression of endoplasmic reticulum (ER) stress‑ and apoptosis‑related proteins was detected by western blotting or immunofluorescence. Reactive oxygen species (ROS) were evaluated by 2',7'‑dichlorofluorescein diacetate fluorescence staining. The results of the present study revealed that BBR treatment decreased PA‑induced podocyte apoptosis. In addition, 4‑phenylbutyric acid significantly reduced PA‑induced cell apoptosis and the expression of ER stress‑related proteins, which indicated that ER stress was involved in PA‑induced podocyte apoptosis. In addition, N‑acetylcysteine inhibited PA‑induced excessive ROS production, ER stress and cell apoptosis of podocytes. BBR also significantly reduced PA‑induced ROS production and ER stress in podocytes. These results suggested that PA mediated podocyte apoptosis through enhancing ER stress and the production of ROS. In conclusion, BBR may protect against PA‑induced podocyte apoptosis, and suppression of ROS‑dependent ER stress may be the key mechanism underlying the protective effects of BBR.While there are numerous small molecule inhibitory drugs available for a wide range of signalling pathways, at present, they are generally not used in combination in clinical settings. Previous reports have reported that the effects of glycogen synthase kinase (GSK)3β, p38MAPK, mTOR and histone deacetylase signaling combined together to suppress the stem‑like nature of hematopoietic stem cells (HSCs), driving these cells to differentiate, cease proliferating and thereby impairing normal hematopoietic functionality. The present study aimed to determine the effect of HDACs, mTOR, GSK‑3β and p38MAPK inhibitor combinations on the efficient expansion of HSCs using flow cytometry. Moreover, it specifically aimed to determine how inhibitors of the GSK3β signaling pathway, in combination with inhibitors of P38MAPK and mTOR signaling or histone deacetylase (HDAC) inhibitors, could affect HSC expansion, with the goal of identifying novel combination strategies useful for the expansion of HSCs.  https://www.selleckchem.com/products/unc-3230.html  The results indicated that p38MAPK and/or GSK3β inhibitors increased Lin‑ cell and Lin‑Sca‑1+c‑kit+ (LSK) cell numbers . These findings further indicated that the suppression of p38MAPK and/or GSK3β signalling may modulate HSC differentiation and self‑renewal to enhance HSC expansion.Increasing evidence has demonstrated that long non‑coding RNAs (lncRNAs) serve important roles in numerous malignancies, including triple‑negative breast cancer (TNBC). The lncRNA titin‑antisense RNA1 (TTN‑AS1) has previously been reported to promote tumorigenesis in various types of cancer. The present study aimed to investigate the potential role of TTN‑AS1 in breast cancer and the associated underlying mechanisms. Following prediction by Starbase and confirmation by dual‑luciferase reporter assay, TINCR was demonstrated to be a target gene for microRNA (miR)‑211‑5p. The expression levels of TTN‑AS1 and miR‑211‑5p, which was predicted to be targeted by TTN‑AS1, in TNBC tissues and in the breast cancer cell lines MDA‑MB‑453 and MDA‑MB‑231 were measured using reverse transcription‑quantitative PCR. Following TTN‑AS1‑knockdown, cell proliferation was measured using a Cell Counting Kit‑8 assay and colony formation assay, whereas cell invasion and migration were measured using Transwell and wound healing assays, respectively.