Aims Increasing evidence indicates that neuroinflammatory and oxidative stress play two pivotal roles in cognitive impairment after surgery. Honokiol (HNK), as an activator of Sirtuin3 (SIRT3), has potential multiple biological functions. The aim of these experiments is to evaluate the effects of HNK on surgery/anesthesia‐induced cognitive decline in mice. Methods Adult C57BL/6 mice received a laparotomy under sevoflurane anesthesia and HNK or SIRT3 inhibitor (3‐TYP) treatment. Cognitive function and locomotor activity of mice were evaluated using fear conditioning test and open field test on postoperative 1 and 3 days. Neuronal apoptosis in CA1 and CA3 area of hippocampus was examined using TUNEL assay. And Western blot was applied to measure the expression of pro‐inflammatory cytokines and SIRT3/SOD2 signaling‐associated proteins in hippocampus. Meanwhile, SIRT3 positive cells were calculated by immunohistochemistry. The mitochondrial membrane potential, malondialdehyde (MDA), and mitochondrial radical oxygen species (mtROS) were detected using standard methods. Results Honokiol attenuated surgery‐induced memory loss and neuronal apoptosis, decreased neuroinflammatory response, and ameliorated oxidative damage in hippocampus. Notably, surgery/anesthesia induced an obviously decrease in hippocampal SIRT3 expression, whereas the HNK increased SIRT3 expression and thus decreased the acetylation of superoxide dismutase 2 (SOD2). However, 3‐TYP treatment inhibited the HNK's rescuing effects. Conclusions These results suggested that activation of SIRT3 by honokiol may attenuate surgery/anesthesia‐induced cognitive impairment in mice through regulation of oxidative stress and neuroinflammatory in hippocampus.

Postoperative delirium (POD) is a common complication following surgery and anesthesia (Surgery/Anesthesia). Mitochondrial dysfunction, which is demonstrated by energy deficits and excessively activated oxidative stress, has been reported to contribute to POD. The dynamic balance between mitochondrial fusion and fission processes is critical in regulating mitochondrial function. However, the impact of Surgery/Anesthesia on mitochondrial fusion/fission dynamics remains unclear. Here, we evaluate the effects of laparotomy under 1.4% isoflurane anesthesia for 2 hours on mitochondrial fission/fusion dynamics in the brain of aged mice. Mice in Surgery/Anesthesia group showed unbalanced fission/fusion dynamics, with decreased DISC1 expression and increased expression of Drp1 and Mfn2 in the mitochondrial fraction, leading to excessive mitochondrial fission and disturbed mitochondrial morphogenesis in the hippocampus and prefrontal cortex. In addition, surgical mice presented mitochondrial dysfunction, demonstrated by abnormally activated oxidative stress (increased ROS level, decreased SOD level) and energy deficits (decreased levels of ATP and MMP). Surgery/Anesthesia also decreased the expression of neuronal/synaptic plasticity-related proteins such as PSD-95 and BDNF. Furthermore, Surgery/Anesthesia induced delirium-like behavior in aged mice. In conclusion, Surgery/Anesthesia disturbed mitochondrial fission/fusion dynamics and then impaired mitochondrial function in the brain of aged mice; these effects may be involved in the underlying mechanism of POD.

Background. The potential mechanism of postoperative cognitive impairment is still largely unclear. The activation of NLRP3 inflammasome had been reported to be involved in neurodegenerative diseases, including postoperative cognitive change, and is closely related to mitochondrial ROS and mitophagy. Honokiol (HNK) owns multiple organic protective effects. This study is aimed at observing the neuroprotective effect of HNK in postoperative cognitive change and examining the role of HNK in the regulation of mitophagy and the relationship between these effects and NLRP3 inflammasome activation in mice induced by surgery/anesthesia. Methods. In this study, mice were divided into several groups: control group, surgery group, surgery+HNK group, and surgery+HNK+3-methyladenine (3-MA) group. Hippocampal tissue samples were harvested and used for proinflammatory cytokines, mitochondrial ROS, and malondialdehyde (MDA) assay. The process of mitophagy and the activation of NLRP3 inflammasome were observed by Western blot, immunohistochemistry, and transmission electron microscopy. Results. The results showed that HNK treatment obviously recovered the postoperative decline and enhanced the expressions of LC3-II, Beclin-1, Parkin, and PINK1 at protein levels after surgery/sevoflurane treatment, which are both an autophagy marker and a mitophagy marker. In addition, HNK attenuated mitochondrial structure damage and reduced mtROS and MDA generation, which are closely associated with NLRP3 inflammasome activation. Honokiol-mediated mitophagy inhibited the activation of NLRP3 inflammasome and neuroinflammation in the hippocampus. Using 3-MA, an autophagy inhibitor, the neuroprotective effects of HNK on mitophagy and NLRP3 inflammasome activation were eliminated. Conclusion. These results indicated that HNK-mediated mitophagy ameliorates postoperative cognitive impairment induced by surgery/sevoflurane. This neuroprotective effect may be involved in inhibiting the activation of NLRP3 inflammasome and suppressing inflammatory responses in the hippocampus.

Background: Alzheimer's disease, the most common form of dementia, has tremendous social and economic impact worldwide. This study aimed to analyze global trends in Alzheimer's disease research and to investigate China's contribution to this research. Methods: The quantity and influence of publications related to Alzheimer's disease in China and elsewhere were compared. The Web of Science (WOS) and PubMed databases were searched from 1988 to 2017 using the terms “Alzheimer's disease” or “Alzheimers disease.” Global Alzheimer's disease publications were classified and analyzed. Keywords, countries, and institutions publishing articles on Alzheimer's disease were analyzed, and citations of these articles were examined. Results: A total of 181,116 articles regarding Alzheimer's disease research were identified and analyzed. Neuroscience and neurology were the main research categories both globally and in China. Basic research dominated Alzheimer's publications, accounting for 30.93% of global publications and 95.31% of publications in China. A total of 8,935 journals published articles related to Alzheimer's disease. The journal Neurobiology of Aging published the most Alzheimer's disease-related articles, numbering 5,206 over the time period examined. The National Institutes of Health, the National Institute on Aging, and the Department of Health and Human Services jointly sponsored 11,809 articles, ranking first in the world. The National Natural Science Foundation of China funded the largest number of studies on Alzheimer's disease in China and recognized the importance of traditional Chinese medicine in Alzheimer's disease research. Conclusions: The present study provides data for global researchers to understand research perspectives and develop future research directions. In recent years, Chinese researchers have contributed significantly to global Alzheimer's research. Still, strengthening international cooperation could improve the quality and number of publications regarding Alzheimer's disease.

BackgroundThere has been tremendous change on neuropathic pain research in the past 20 years in China and around the world. We analyzed the global trend of neuropathic pain research and compared China’s quantity and quality of neuropathic pain-related publications with other developed countries.MethodsUsing terms “neuropathic pain”, we retrieved related publications from the Web of Science (WOS) database and PubMed database. From different aspects, such as the number of papers, total citations, average citations per item, H-index, research types, orientation, institutions, journals and funding, global neuropathic pain publications were classified and analyzed.ResultsFrom 1998 to 2017, 21,733 articles regarding neuropathic pain research were published worldwide. Of these, 9.394% were contributed by authors from Chinese institutions, which followed USA and ranked second. However, the quality indicators of publications, including total citations, average citations per item and H-index, were relatively low in China. High contribution journals and the 10 most-cited articles on neuropathic pain in world and China were also listed, which also can reflect the quality of neuropathic pain. Based on National Natural Science Foundation of China (NSFC), basic research was the main articles type, accounting for 32.91% of China’s neuropathic pain research.ConclusionGlobal neuropathic pain research increased rapidly during the 1998 to 2017 period. The USA was still the leader of neuropathic research. Although China had made great achievements, there was a significant gap in the high-quality studies between China and other leading countries.

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These results suggest that propofol, at clinically relevant concentrations, can reduce inflammatory responses in LPS-induced inflammation in activated microglia and might be an intravenous anesthetic of choice when patients with neuroinflammatory diseases require sedation and/or general anesthesia.

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