BackgroundChinese medical universities typically have a high number of students, a shortage of teachers and limited equipment, and as such histology courses have been taught using traditional lecture-based formats, with textbooks and conventional microscopy. This method, however, has reduced creativity and problem-solving skills training in the curriculum. The virtual microscope (VM) system has been shown to be an effective and efficient educational strategy. The present study aims to describe a VM system for undergraduates and to evaluate the effects of promoting active learning and problem-solving skills.MethodsTwo hundred and twenty-nine second-year undergraduate students in the Third Military Medical University were divided into two groups. The VM group contained 115 students and was taught using the VM system. The light microscope (LM) group consisted of 114 students and was taught using the LM system. Post-teaching performances were assessed by multiple-choice questions, short essay questions, case analysis questions and the identification of structure of tissue. Students’ teaching preferences and satisfaction were assessed using questionnaires.ResultsTest scores in the VM group showed a significant improvement compared with those in the LM group (p < 0.05). There were no substantial differences between the two groups in the mean score rate of multiple-choice questions and the short essay category (p > 0.05); however, there were notable differences in the mean score rate of case analysis questions and identification of structure of tissue (p < 0.05). The questionnaire results indicate that the VM system improves students’ productivity and promotes learning efficiency. Furthermore, students reported other positive effects of the VM system in terms of additional learning resources, critical thinking, ease of communication and confidence.ConclusionsThe VM system is an effective tool at Chinese medical university to promote undergraduates’ active learning and problem-solving skills as an assisted teaching platform.
As one of the fundamental components of Astragalus membranaceus, astragaloside IV (AST IV) exerts protective effects against cerebral ischemia-reperfusion injury (CIRI). Nevertheless, the underlying mechanisms have not yet been conclusively elucidated. To do so, here, we report on the regulatory effects of Nrf2 on NLRP3 inflammasome-mediated pyroptosis. CIRI was induced by middle cerebral artery occlusion-reperfusion (MCAO/R) in Sprague Dawley rats and modeled by oxygen and glucose deprivation/reoxygenation (OGD/R) in SH-SY5Y cells. Cerebral infarct volume and neurological deficit score served as indices to evaluate MCAO/R injury. In addition, the CCK-8 assay was used to assess cell viability, the LDH leakage rate was used as a quantitative index, and propidium iodide (PI) staining was used to visualize cells after OGD/R injury. The NLRP3/Caspase-1/GSDMD pathway, which produces the pores in the cell membrane that are central to the pyroptosis process, was assessed to investigate pyroptosis. Nrf2 activation was assessed by detecting Nrf2 protein levels and immunofluorescence analysis. We show that after MCAO/R of rats, the infarct volume and neurological deficit score of rats were strongly increased, and after OGD/R of cell cultures, cell viability was strongly decreased, and the LDH leakage rate and the proportion of PI-positive cells were strongly increased. In turn, MCAO/R and OGD/R enhanced the protein levels of NLRP3, Caspase-1, IL-1β, GSDMD, and GSDMD-N. Moreover, Nrf2 protein levels increased, and Nrf2 translocation was promoted after CIRI. Interestingly, AST IV (i) reduced the cerebral infarct volume and the neurological deficit score in vivo and (ii) increased the cell viability and reduced the LDH leakage rate and the proportion of PI-positive cells in vitro. AST IV reduced the protein levels of NLRP3, Caspase-1, IL-1β, GSDMD, and GSDMD-N, inhibiting NLRP3 inflammasome-mediated pyroptosis. AST IV also increased the protein levels of Nrf2 and promoted the transfer of Nrf2 to the nucleus, accelerating Nrf2 activation. Particularly revealing was that the Nrf2 inhibitor ML385 partly blocked the above effects of AST IV. Taken together, these results demonstrate that AST IV alleviates CIRI through inhibiting NLRP3 inflammasome-mediated pyroptosis via activating Nrf2.
Background It was indicated that nucleotide-binding oligomerisation domain‑like receptor protein 1 (NLRP1) inflammasome-mediated pyroptosis is involveg in the progression of Alzheimer’s disease (AD). This study was designed to explore the effect of Bushen Huoxue Acupuncture on cognitive defect and NLRP1 inflammasome-mediated pyroptosis in AD mouse. Methods Senescence-accelerated mouse prone 8 (SAMP8) mice were used as a model of AD. Bushen Huoxue Acupuncture was performed in four acupoints: “Baihui acupoint” (GV20), “Shenshu acupoint” (BL23), “Xuehai acupoint” (SP10), and “Geshu acupoint” (BL17). Morris water maze test was performed to evaluate the cognitive function of the mouse. The levels of Aβ 1-40 , Aβ 1-42 , IL-1β, and IL-18 were examined by ELISA assay. Neuronal apoptosis and damage in hippocampal tissues were measured using TUNEL and Nissl staining, respectively. The expression of NLRP1, ASC, cleaved caspase-1, IL-1β, and IL-18 was examined using Western blot. Results Bushen Huoxue Acupuncture improved the learning and memory deficits of AD mouse. Meanwhile, Bushen Huoxue Acupuncture decreased the production of Aβ in hippocampal tissues of SAMP8 mice and attenuated the neuronal apoptosis and damage. Furthermore, Bushen Huoxue Acupuncture inhibited NLRP1 inflammasome activation in SAMP8 mice. Conclusion Bushen Huoxue Acupuncture could notably attenuate the cognitive defect of mouse AD model and inhibit NLRP1 inflammasome-mediated pyroptosis.
Background. EA therapy is a traditional therapeutic approach for alleviation of cerebral I/R-induced brain injury. We investigated the effect of EA on MCAO rat model to examine the mechanism of apoptosis in the rat hippocampus. Methods. 200 male Sprague-Dawley rats were randomly divided into sham, I/R, EA, ERK inhibitor (PD), and ERK inhibitor+EA (PD+EA) groups. Each group was subdivided into 5 groups according to different time points. Locomotor behaviors were evaluated using neurological scales and morphological examination was performed using HE staining. Apoptosis index of neural cells in local infarcted area was measured by TUNEL and p-ERK expression was detected using immunohistochemistry technique and western blot analysis. Results. Neurological deficit scores and neural apoptosis in the EA group were lower than I/R group at the same time points, respectively. At different time points, p-ERK level was increased in the ischemic hippocampal CA1 in the EA group as compared to I/R group; the increased level was increased most at 1 day, 3 days, and 1 week (p < 0.01). Conclusion. EA alleviates neurological deficit, reduces apoptosis index, and simultaneously upregulates the expression of p-ERK signal pathway in rats subjected to I/R injury.
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