RESUMO
Background: Recently, multiple preclinical studies have reported the beneficial effect of berberine in the treatment of Alzheimer's disease (AD). Nevertheless, the neuroprotective effects and possible mechanisms of berberine against AD are not universally recognized. This study aimed to conduct a systematic review and meta-analysis by integrating relevant animal studies to assess the neuroprotective effects and potential mechanisms of berberine on AD. Methods: We systematically searched PubMed, Embase, Scopus and Web of Science databases that reported the effects of berberine on AD models up to 1 February 2023. The escape latency, times of crossing platform, time spent in the target quadrant and pro-oligomerized amyloid beta 42 (Aß1-42) were included as primary outcomes. The secondary outcomes were the Tau-ps 204, Tau-ps 404, ß-site of APP cleaving enzyme (BACE1), amyloid precursor protein (APP), acetylcholine esterase (AChE), tumor necrosis factor ⺠(TNF-α), interleukin 1ß (IL-1ß), IL-6, nitric oxide (NO), glial fibrillary acidic protein (GFAP), malonaldehyde (MDA), glutathione S-transferase (GST), glutathione (GSH), glutathione peroxidase (GPx), Beclin-1 and neuronal apoptosis cells. This meta-analysis was conducted using RevMan 5.4 and STATA 15.1. The SYRCLE's risk of bias tool was used to assess the methodological quality. Results: Twenty-two studies and 453 animals were included in the analysis. The overall results showed that berberine significantly shortened the escape latency (p < 0.00001), increased times of crossing platform (p < 0.00001) and time spent in the target quadrant (p < 0.00001), decreased Aß1-42 deposition (p < 0.00001), Tau-ps 202 (p < 0.00001) and Tau-ps 404 (p = 0.002), and improved BACE1, APP, AChE, Beclin-1, neuronal apoptosis cells, oxidative stress and inflammation levels. Conclusion: Berberine may be a promising drug for the treatment of AD based on preclinical evidence (especially when the dose was 5-260 mg/kg). The potential mechanisms for these protective effects may be closely related to anti-neuroinflammation, anti-oxidative stress, modulation of autophagy, inhibition of neuronal apoptosis and protection of cholinergic system. However, these results may be limited by the quality of existing research. Larger and methodologically more rigorous preclinical research are needed to provide more convincing evidence.
RESUMO
BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases in the world that represents an important public health challenge nowadays. Lifestyle changes and exercise can reduce the development of fatty liver. The aim of this systematic review and meta-analysis is to evaluate the treatment efficacy of Qigong for NAFLD. METHODS: A detailed search for articles up to September 2020 will be performed to identify randomized controlled trials for Qigong in NAFLD. The following database will be used: PUBMED, Embase, Web of Science, Cochrane Library, Sino Med, Chinese National Knowledge Infrastructure (CNKI), Chinese Science and Technology Periodicals Database, and Wanfang Databas. Grey literature will be explored and the selection of studies, data extraction and validation will be performed independently by 2 reviewers using predefined selection criteria and quality indicators. Stata V.13.0 and Review manager 5.3 software will be used for data synthesis, sensitivity analysis, subgroup analysis, and risk of bias assessment. We will use the grading of recommendations assessment, development, and evaluation system to assess the quality of evidence. RESULTS: This research will provide a quantitative and standardized assessment of the treatment efficacy of Qigong for NAFLD. CONCLUSION: This systematic review will generate the latest evidence for determining whether Qigong has a positive treatment effect for NAFLD. REGISTRATION NUMBER: INPLASY202090034.
