AI辅助文献解读｜脂代谢参与缺血性卒中的神经修复

AI辅助文献解读｜脂代谢参与缺血性卒中的神经修复

随着AI工具的普及，给我们的科研生活带来了许多便利。AI在辅助文献阅读这一方面，因其具备快速阅读提炼文字的功能，被人们使用的广泛，为众多科研工作者节省了宝贵的时间，让大家可以“偷个懒”。

AI辅助文献解读，可以用于我们进行文献调研，组会文献汇报，对某领域大量文献的摘要或研究背景等总结，数据结果的解读….用途多多，然而准确性还是有待提高。

有些时候，需要快速了解多篇文献的研究背景或者是汇报存在DDL，自己阅读效率太低，想走捷径省力，但又担心AI乱解读不靠谱，不知道如何使用AI来辅助。那么，今天我将就Takashi Shichita 团队在《Neuron》上发表题为 “PLA2G2E-mediated lipid metabolism triggers brain autonomous neural repair after ischemic stroke” 的这篇文章，结合AI工具，来一起测试一下AI到底靠不靠谱，哪些是准确的。

引言原文

Introduction In today's aging society, a large number of patients around the world suffer from neurological sequelae of brain tissue injury, including those brought about by major strokes. 1,2,3 Although the lost brain functions due to brain injury are often poorty recoverable, rehabilitation can improve patients' functional prognosis to some extent,4,5,6 suggesting the existence of cerebral self-recovery mechanisms after injury.7,8,9 Nervous system reconstruction, synapse organization, and remyelination are implicated in these recovery processes, which are induced by the various neurotrophins or factors regulating neurite projection or synaptogenesis around the injured region. 10,11,12,13 The neurons surrounding the injured region must not only survive despite injury stresses but also acquire reparative functions for efficient functional recovery.14 The triggering molecular mechanisms that induce this broad range of neural repair after brain injury remain to be clarified.15,16 Necrotic cell death after injuries has broad effects; for example, the extracellular release of endogenous molecules called alarmin from dead cells is generally inflammatogenic. 17,18 We previously identified the peroxiredoxin (PRX) family proteins and DJ-1 (PARK7) released extracellularly from dead neurons as damage-associated molecular patterns (DAMPs) that directly activate infiltrating immune cells to produce inflammatory cytokines, 19,20 and their removal through scavenger receptors, macrophage scavenger receptor 1 (MSR1) or macrophage receptor with collagenous structure (MARCO), resolves cerebral inflammation after ischemic brain injury.21 Classically, various lipid mediators generated after tissue injuries are well known to regulate inflammation. Prostaglandins and leukotrienes, metabolites of w6 arachidonic acid (AA; C20:4), are well- known pro-inflammatory lipid mediators.22,23 By contrast, resolvins, neuroprotectin D1, and maresins metabolites of w3 eicosapentaenoic acid (EPA; C20:5) or docosahexaenoic acid (DHA; C22:6) have recently been identified as pro-resolving lipid mediators.23,24,25 These polyunsaturated fatty acids (PUFAs) and their metabolites are generated by the enzymatic activities of the various PLA2 subtypes from the phospholipids included in the cellular membrane or membranous debris after tissue injuries.26,27,28 Among approximately fifty subtypes of PLA2, only PLA2G4A has been known to generate inflammatory lipid mediators in ischemic stroke, 22,23 whereas the functions of other PLA2 subtypes remain to be clarified. Nevertheless, few cerebral endogenous molecules that trigger a broad range of neural repair after brain injury have been identified. These endogenous molecules are expected to be pro-survival and pro-reparative for the neurons around the injured region and to accelerate stroke recovery. In this study, we discovered the pivotal roles of the secreted phospholipase PLA22E from neurons that induced peptidyl arginine deiminase 4 (PADI4) expression to grant pro-survival and pro-reparative functions in peri-infarct neurons after ischemic brain injury. Neuronal PADI4 was important not only for preventing additional cell death and subsequent severe inflammation but also for inducing the peri-infarct neuronal populations bearing gene expression profiles associated with recovery processes after brain injury.

我们可以将引言原文的内容复制到对话框，输入指令：用医学术语翻译成中文，再分点总结研究背景。这样可以帮助我们快速判断生成的答案是否是正确的，一般来说，不同的AI及翻译软件，可能在语法、专业词语等方面存在差异，但是对内容的总体把握及理解是一致的。我们可以对翻译后的内容及答案进行比对：

1. 是否是根据给出的内容体检总结的，检验答案的匹配度
2. 答案是否过于空洞，不够具体，优化提问方式及指令，提高AI智能度

下面是行学AI给出的答案：

那我们可以看到，它的回答是基于文本的，并且是按照顺序进行总结的，但是稍微显得不那么具体，这时候我们进行指令优化，参考如下：分段具体总结引言部分生成3段文字，要求补充细节内容，按照小标题：具体内容进行展示

这时候可以看出，相较于之前的指令，文本的格式及内容丰富度都得到了改善。

原文的引言部分的研究思路如下，可以看到AI给出的答案还是值得借鉴的：

1. 老龄化社会背景

   ├── 神经系统损伤影响广泛

   │   ├── 由重大中风引起的损伤

   │   ├── 功能恢复难度大

   │   └── 康复治疗改善功能预后

   └── 存在自恢复机制

       ├── 神经系统重建

       ├── 突触组织

       └── 再髓鞘化

2. 神经元适应与修复机制

   ├── 受损区域的神经元

   │   ├── 面对伤害压力

   │   └── 必须获得修复功能

   └── 诱发神经修复的分子机制待澄清

3. 细胞死亡及其影响

   ├── 坏死细胞释放内源性分子

   │   ├── 促炎特性（alarmin）

   │   ├── 激活免疫细胞，产生炎性细胞因子

   │   └── 清道夫受体用于缓解炎症

   ├── 脂质介导物的研究

   │   ├── 促炎脂质介导物（前列腺素、白三烯）

   │   └── 促缓解脂质介导物（解决因子、神经保护素D1、马瑞辛）

   └── PLA2亚型的角色

       ├── 约五十种PLA2亚型

       ├── PLA2G4A与炎症脂质介导物生成相关

       └── 其他亚型的功能待进一步研究

4. 内源性修复分子的发现

   ├── 有效的内源性分子较少

   │   ├── 促进受损区域神经元存活和修复

   │   └── 加速中风恢复

   └── PLA2G2E的关键作用

       ├── 从神经元中分泌

       ├── 诱导PADI4表达

       │   ├── 促进存活

       │   ├── 防止额外细胞死亡

       │   └── 诱导相关基因表达特征

       └── 生成DGLA和15-HETrE以诱导PADI4表达

今天的分享就到此结束啦，希望大家善用AI，顺利科研。