Background: Virtual reality (VR) is an innovation that permits the individual to discover and operate within threedimensional (3D) environment to gain practical understanding. This research aimed to examine the general efficiency of VR for teaching medical anatomy. Methods: We executed a meta-analysis of randomized controlled studies of the performance of VR anatomy education. We browsed five databases from the year 1990 to 2019. Ultimately, 15 randomized controlled trials with a teaching outcome measure analysis were included. Two authors separately chose studies, extracted information, and examined the risk of bias. The primary outcomes were examination scores of the students. Secondary outcomes were the degrees of satisfaction of the students. Random-effects models were used for the pooled evaluations of scores and satisfaction degrees. Standardized mean difference (SMD) was applied to assess the systematic results. The heterogeneity was determined by I 2 statistics, and then was investigated by meta-regression and subgroup analyses. Results: In this review, we screened and included fifteen randomized controlled researches (816 students). The pooled analysis of primary outcomes showed that VR improves test scores moderately compared with other approaches (standardized mean difference [SMD] = 0.53; 95% Confidence Interval [CI] 0.09-0.97, p < 0.05; I 2 = 87.8%). The high homogeneity indicated that the studies were different from each other. Therefore, we carried out metaregression as well as subgroup analyses using seven variables (year, country, learners, course, intervention, comparator, and duration). We found that VR improves post-intervention test score of anatomy compared with other types of teaching methods. Conclusions: The finding confirms that VR may act as an efficient way to improve the learners' level of anatomy knowledge. Future research should assess other factors like degree of satisfaction, cost-effectiveness, and adverse reactions when evaluating the teaching effectiveness of VR in anatomy.

Stroke is a complex disease involved oxidative stress-related pathways in its pathogenesis. The nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway has been considered a potential target for neuroprotection in stroke. Acetyl-11-Keto-β-Boswellic Acid (AKBA) is an active triterpenoid compound from the extract of Boswellia serrate. The present study was to determine whether AKBA, a novel Nrf2 activator, can protect against cerebral ischemic injury. The stroke model was produced in Sprague–Dawley rats via middle cerebral artery occlusion. To model ischemia-like conditions in vitro, primary cultured cortical neurons were exposed to transient oxygen and glucose deprivation (OGD). Treatment of AKBA significantly reduced infarct volumes and apoptotic cells, and also increased neurologic scores by elevating the Nrf2 and HO-1 expression in brain tissues in middle cerebral artery occlusion (MCAO) rats at 48 hours post reperfusion. In primary cultured neurons, AKBA increased the Nrf2 and HO-1 expression, which provided protection against OGD-induced oxidative insult. Additionally, AKBA treatment increased Nrf2 binding activity to antioxidant-response elements (ARE). The protective effect of AKBA was attenuated by knockdown of Nrf2 or HO-1. In conclusion, these findings provide evidence that AKBA protects neurons against ischemic injury, and this neuroprotective effect involves the Nrf2/HO-1 pathway.

Oxidative stress is well known to play a pivotal role in cerebral ischemia-reperfusion injury. The nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway has been considered a potential target for neuroprotection in stroke. 11-Keto-β-boswellic acid (KBA) is a triterpenoid compound from extracts of Boswellia serrata. The aim of the present study was to determine whether KBA, a novel Nrf2 activator, can protect against cerebral ischemic injury. Middle cerebral artery occlusion (MCAO) was operated on male Sprague-Dawley rats. KBA (25 mg/kg) applied 1 h after reperfusion significantly reduced infarct volumes and apoptotic cells as well as increased neurologic scores at 48 h after reperfusion. Meanwhile, posttreatment with KBA significantly decreased malondialdehyde (MDA) levels, restored the superoxide dismutase (SOD) activity, and increased the protein Nrf2 and HO-1 expression in brain tissues. In primary cultured astrocytes, KBA increased the Nrf2 and HO-1 expression, which provided protection against oxygen and glucose deprivation (OGD)-induced oxidative insult. But knockdown of Nrf2 or HO-1 attenuated the protective effect of KBA. In conclusion, these findings provide evidence that the neuroprotection of KBA against oxidative stress-induced ischemic injury involves the Nrf2/HO-1 pathway.