Molecular medicine reports
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The present study investigated the effect of dexmedetomidine on hippocampal inflammation and cognitive function in rats with postoperative cognitive dysfunction (POCD). A total of 80 healthy male Sprague Dawley rats were used, 72 of which developed POCD. The rats were randomly divided into four groups: The control, model, low‑dose and high‑dose dexmedetomidine anesthesia groups. ⋯ Additionally, on the first day after surgery, the expression levels of IL‑1β, TNF‑α and NF‑κB in the hippocampi of rats in the low‑ and high‑dose dexmedetomidine anesthesia groups were significantly lower than those in the model group, and the decrease was more pronounced in the high‑dose group. At 7 days after surgery, the differences in expression levels of IL‑1β, TNF‑α and NF‑κB in the hippocampus among groups were not identified to be statistically significantly different. Taken together, the results of the present study indicated that dexmedetomidine may inhibit hippocampal inflammation induced by surgical trauma, and that dexmedetomidine may effectively improve postoperative cognitive function in rats.
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Myocardial infarction (MI) is associated with a high risk of mortality and is a major global health concern. The present study aimed to investigate the protective effects of (3R)‑5,6,7‑trihydroxy‑3‑isopropyl‑3‑methylisochroman‑1‑one (TIM) against MI induced by isoproterenol (ISO) in a rat model and the underlying mechanisms. Wistar rats were assigned to 4 groups (n=10): The control group received saline treatment; the ISO group received an intraperitoneal injection of ISO (100 mg/kg); and the TIM (low) and TIM (high) groups received an intraperitoneal injection of ISO, plus a 1 and 2 mg/kg dose of TIM orally, respectively. ⋯ Furthermore, treatment with TIM upregulated the levels of apelin in the plasma and myocardium of ISO‑treated rats. The results indicated that TIM protected cardiomyocytes against ISO‑induced MI, potentially via the apelin/apelin receptor signaling pathway. The results of the present study suggested that TIM may be a potential novel therapy for the treatment of MI.
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Despite the various different candidate genetic polymorphisms of potential clinical relevance, there is not enough understanding of the inter‑individual variability in analgesic administration. The cytochrome P450 2D6 (CYP2D6) genotype is thought to be one of the most studied. The aim of the present evidence‑based review was to determine if there is now sufficient evidence to make clinical recommendations based on a specific genomic profile. ⋯ Finally, polymorphisms of the ATP‑binding cassette family of efflux transporters were highlighted. Consistent data on pain polymorphisms is now widely available; however, these results have had very little impact on clinical guidelines and daily oncologist practice. Persisting pain, side effects of grade 3 (NCI‑CTCAE v4.0) and breakthrough pain with more than 4 episodes/day should be considered the criteria for pain multidisciplinary team discussions and for polymorphism screening.
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Traditional herbal medicines are being increasingly used worldwide to treat cancer. Radix Sophorae Flavescentis (RSF) is a Chinese herb, which has numerous pharmacological properties, including anti‑tumour effects. In this study, we investigated the mechanisms underlying RSF‑induced apoptosis in human gastric cancer cells (AGS cells). ⋯ In addition to increasing the expression levels of apoptosis‑mediating surface antigen FAS and Fas ligand, RSF also activated caspase‑3; however, mitogen‑activated protein kinase appeared to inhibit RSF‑induced cell death. RSF also led to an increased production of reactive oxygen species. Based on these results, we propose that RSF could be a potential therapeutic agent for gastric cancer.
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Increasing cell apoptosis is one of the major causes of intervertebral disc degeneration (IDD). β-ecdysterone has been demonstrated to protect PC12 cells against neurotoxicity. A previous study revealed that β‑ecdysterone may be involved in the regulation of autophagy in osteoblasts. Therefore, we hypothesized that β‑ecdysterone may possess therapeutic effects on IDD via autophagy stimulation. ⋯ Inhibition of autophagy with 3‑methyladenine partially abrogated the protective function of β‑ecdysterone against apoptosis of nucleus pulposus cells, indicating that autophagy participated in the protective effect of β‑ecdysterone on IDD. Additionally, β‑ecdysterone promoted the expression of anabolic genes while inhibiting the expression of catabolic genes in nucleus pulposus cells. Collectively, the present study demonstrated that β‑ecdysterone may protect nucleus pulposus cells against apoptosis by autophagy stimulation and ameliorate disc degeneration, which indicates that β‑ecdysterone may be a potential therapeutic agent for IDD.