Skin aging is intricately linked to age-associated inflammation. Nicotine, as a potential anti-inflammatory agent, may exert anti-aging effects by modulating inflammatory responses. This study aims to explore whether nicotine can mitigate skin aging and associated with the activation of the cholinergic anti-inflammatory pathway (CAP) mediated by the α7 nicotinic acetylcholine receptor (α7nAChR). The results showed that a significant reduction in the expression of α7nAChR both in the skins of elderly individuals and rats with advancing age, which is accompanied by an increase in inflammatory markers and oxidative stress. Following nicotine intervention, the α7nAChR was activated, leading to inhibition of the NF-κB signaling cascades and the activity of matrix metalloproteinases, as well as degradation of collagen fibers in aged skin. But nicotine co-treatment with the α7nAChR antagonist methyllycaconitine (MLA), its abilities to delay skin structural degradation were obvious weakened. The results First time showed that the α7nAChR deficiency both in human and rats’ skin with age, nicotine can effectively improve the degradation of skin structure and functional integrity mediates by α7nAChR anti- inflammation pathway. This suggests potential therapeutic strategies for combating skin aging and related pathologies.

Vascular aging is recognized as critical factor contributing to the onset and progression of cardiovascular diseases, which represent a leading cause of morbidity and mortality worldwide. The α7 nicotinic acetylcholine receptor (α7nAChR) exhibits widespread expressed in the cardiovascular system and is intricately linked to a diverse array of pathologies, in cardiovascular, conditions. Research indicates that oxidative stress plays a crucial role in exacerbating endothelial dysfunction and promoting vascular aging. However, less is known regarding the role of α7nAChR in vascular aging. In this study, we employed a combination of cellular experiments, animal models, and molecular biological techniques, utilizing an agonist (PNU282987) and antagonists (Malondialdehyde, MLA) of α7nAChR as pharmacological tools to investigate the role of α7nAChR in aging-related pathologies. The expression of α7nAChR in vascular tissue decreases with age both in rats and humans. Activation of α7nAChR alleviated vascular aging in aged rats, as evidenced by improving endothelium-dependent vasodilatation and endothelial continuity, decreased senescence-associated β-galactosidase activity, phosphorylation of H2A.XSer139, expression of p21 and p16INK4a and inflammation, Notably, effective activation of the α7nAChR mediated Nrf2/HO-1 signaling pathway and antioxidant activity by specific agonist, PNU282987, conversely, which were blocked by the α7nAChR-selective inhibitor MLA. The findings highlight the vital role of α7nAChR receptor in preserving vascular health and endothelial integrity in the development of vascular aging, Consequently, targeting the α7nAChR/Nrf2/HO-1 signaling pathway could serve as a potential therapeutic approach for the development of novel anti-aging strategies.

To investigate the role of intestinal flora and cholinergic anti-inflammatory pathways in the gut-brain axis, using oral gavage and intraperitoneal injection of methyllycaconitine (MLA). MLA was administered at a dose of 4 mg/kg for 30 days, either orally or via intraperitoneal injection. Rats were then assessed for behavioral changes, inflammatory markers, neurotransmitters, neuroreceptors, and intestinal mucosal barrier integrity. Rats receiving MLA via intraperitoneal injection exhibited significant behavioral abnormalities compared to the control and orally administered MLA groups. The levels of IL-1β were elevated in both intestinal and hippocampal tissues, while IL-10 levels were decreased. Brain-derived neurotrophic factor (BDNF) was significantly lower in hippocampal tissues. Furthermore, α7nAChR expression was reduced in hippocampal tissues, accompanied by an increase in 5-HT3A receptors. The intestinal mucosal barrier was compromised, as evidenced by reduced expression of ZO-1 and Occludin, along with increased IL-1β and decreased IL-10 levels in the gut. Our findings suggest that oral gavage of MLA does not induce cognitive impairment in rats compared to intraperitoneal injection, possibly due to the involvement of intestinal flora in the protective effects of CAP.

BACKGROUND:The gut-liver axis, pivotal in managing glucose balance and insulin responsiveness, is central to the development of type 2 diabetes mellitus (T2DM). Research has highlighted the regulatory effects of dietary alpha-linolenic acid (ALA), but it remains unclear how ALA modulates gut microbiota and liver inflammation in T2DM. PURPOSE:This study aimed to systematically investigate ALA's influence on liver inflammation, intestinal barrier integrity, gut microbial composition, and metabolic homeostasis in T2DM, with a focus on the underlying molecular mechanisms. STUDY DESIGN:A dual-model approach was employed using both db/db mouse model and the SCZ/NA-induced T2DM rat model to ensure robust species and model validation. METHODS:Animals received oral ALA supplementation, followed by assessments of glucose tolerance, insulin sensitivity, hepatic histology, and inflammatory markers. Intestinal barrier function, permeability, and systemic LPS levels were evaluated. Mechanistic analysis focused on the GPR120-NF-κB/NLRP3 signaling pathway. Multi-omics profiling including fecal metagenomics, SCFA quantification, and plasma metabolomics were conducted to assess gut microbiota and host metabolic responses. RESULTS:Our results revealed that ALA therapy significantly mitigated insulin resistance and glucose intolerance in db/db mice. Histopathological analysis revealed a decrease in hepatic steatosis following ALA administration, alongside a reduction in inflammatory markers indicative of T2DM. Importantly, our findings demonstrated that ALA mitigates liver inflammation by inhibiting the NF-κB/NLRP3 pathway, possibly via its interaction with GPR120. Beyond this, augmenting ALA bolstered intestinal integrity, minimized permeability, curbed lipopolysaccharide leakage, and suppressed pro-inflammatory cytokine expression within the intestines. Significantly, an integrated multi-omics investigation, encompassing fecal metagenomic sequencing, SCFA evaluation, and plasma non-targeted metabolomics, disclosed a potent correlation between ALA's hypoglycemic efficacy and the modulation of gut microbial community structure, elevation of SCFA synthesis, and enhancement of metabolic signatures. CONCLUSION:Our study's initial insights indicated that dietary ALA modulates inflammation and metabolism in T2DM via the gut-liver axis, specifically through the GPR120-NF-κB/NLRP3 pathway. This elucidates ALA's dual function in reshaping the gut microbiota and combating systemic inflammation, positioning it as a potentially efficacious dietary component for managing T2DM.

Brain aging is a major factor in cognitive decline and Alzheimer’s disease (AD) progression. Aging-induced microglial senescence critically drives inflammaging and brain aging processes. Nevertheless, the underlying reasons and mechanisms that promote microglial aging remain unclear. This study explores how 27-hydroxycholesterol (27-OHC), a key oxysterol, accelerates brain aging by promoting microglial senescence, iron overload, and neuroinflammation. Clinically, we observed a significant inverse correlation between plasma 27-OHC levels and Mini-Mental State Examination (MMSE) scores in AD patients, accompanied by reduced 24S-OHC concentrations. Experimental studies revealed that 27-OHC administration in mice induced hippocampal-dependent cognitive impairment and anxiety-like behaviors, concurrent with elevated expression of cellular senescence markers (P21, P16, SA-β-Gal) and M1 microglial polarization. In BV-2 cells, 27-OHC disrupted iron homeostasis (DMT1/ferritin/GPX4 dysregulation), elevating ROS and impairing mitochondrial function. Deferoxamine (DFX) mitigated microglial senescence and ferroptosis. These findings establish the 27-OHC-iron axis as a novel therapeutic target for combating cholesterol-driven neurodegeneration.

Microglia are the drivers of neuroinflammation. Microglia activation plays a critical role in the pathogenesis of aging. However, the mechanisms underlying microglial activation during aging are still not fully understood. Here, we investigated the role of S-adenosylmethionine (SAM) and its interplay with microglial activation in aging. In this study, we investigated the effect of SAM on BV2 cells treated with D-galactose (D-gal) and its molecular mechanism by Cell Counting Kit-8 (CCK8) assay, Senescence-associated beta-Galactosidase (SA-beta-gal) staining, western blot and immunofluorescence. We found that D-gal could induce microglia senescence. SAM intervention induced a significant decrease in the levels of inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) and increased arginase-1 (Arg1), alpha 7 nicotinic acetylcholine receptor (alpha 7nAChR), nuclear factor erythrocyte 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) expression. Moreover, after administration of alpha 7nAChR selective antagonist methyllycaconitine citrate (MLA), our results showed that SAM enhanced expression of alpha 7nAChR, Nrf2 and HO-1, promoted the transformation of microglia from M1 to M2 subtype, and decreased the proinflammatory cytokines compared with MLA + D-gal group. These results suggest that SAM attenuates neuroinflammation by inhibiting microglia polarization through the alpha 7nAChR/Nrf2/HO-1 pathway.

OBJECTIVE To investigate the role of intestinal flora and cholinergic anti-inflammatory pathways in the gut-brain axis, using oral gavage and intraperitoneal injection of methyllycaconitine (MLA). METHODS MLA was administered at a dose of 4 mg/kg for 30 days, either orally or via intraperitoneal injection. Rats were then assessed for behavioral changes, inflammatory markers, neurotransmitters, neuroreceptors, and intestinal mucosal barrier integrity. RESULTS Rats receiving MLA via intraperitoneal injection exhibited significant behavioral abnormalities compared to the control and orally administered MLA groups. The levels of IL-1β were elevated in both intestinal and hippocampal tissues, while IL-10 levels were decreased. Brain-derived neurotrophic factor (BDNF) was significantly lower in hippocampal tissues. Furthermore, α7nAChR expression was reduced in hippocampal tissues, accompanied by an increase in 5-HT3A receptors. The intestinal mucosal barrier was compromised, as evidenced by reduced expression of ZO-1 and Occludin, along with increased IL-1β and decreased IL-10 levels in the gut. CONCLUSION Our findings suggest that oral gavage of MLA does not induce cognitive impairment in rats compared to intraperitoneal injection, possibly due to the involvement of intestinal flora in the protective effects of CAP.

Oxidative stress and neuroinflammation play crucial roles in aging. S-adenosylmethionine (SAM), a popular supplement, is a potential antioxidant and candidate therapy for depression. This study aimed to evaluate the neuroprotective effects of SAM on D-galactose-induced brain aging and explore its underlying mechanisms. Brain aging model was established with D-galactose (180 mg/kg/day) for 8 weeks. During the last 4 weeks, SAM (16 mg/kg) was co-administrated with D-galactose. Behavior tests were used to assess cognitive function and depression-like behaviors of rats. Results showed that cognitive impairment and depression-like behaviors were reversed by SAM. SAM reduced neuronal cell loss, increased brain-derived neurotrophic factor level in the hippocampus, inhibited amyloid-beta level and microglia activation, as well as pro-inflammatory factors levels in the hippocampus and serum. Further, SAM enhanced antioxidant capacity and attenuated cholinergic damage by reducing malondialdehyde levels, increasing acetylcholine levels, expression levels of alpha 7 nicotinic acetylcholine receptor (alpha 7nAChR), nuclear factor erythrocyte 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) in the hippocampus. Above all, SAM has a potential neuroprotective effect on ameliorating cognitive impairment in brain aging, which is related to inhibition of oxidative stress and neuroinflammation, as well as alpha 7nAChR signals. Data Availability: Data will be made available on request.

观察新生大鼠啶虫脒(acetamiprid,ACE)慢暴露对成年后神经行为、大脑皮质与海马的影响.选择出生一周的雄性Spra-gue-Dawley(SD)大鼠 18 只,随机分为对照组(Control)、ACE-15 组(15 mg·kg-1·d-1)、ACE-40 组(40 mg·kg-1·d-1),每组 6 只.ACE暴露组灌胃干预9周,期间每周检测体质量.采用开放旷场实验(OFT)、Morris水迷宫(MWM)检测大鼠行为学变化;采用试剂盒检测大脑皮质和海马组织中丙二醛(MDA)和超氧化物歧化酶(SOD)水平;采用Western Blot法检测白细胞介素IL-1β、IL-10蛋白表达量;采用苏木精-伊红(H&E)染色法检测大脑皮质和海马组织病理学改变;采用Nissl染色法检测大脑海马DG、CA3区神经元变化.OFT结果显示,与对照组相比,ACE暴露组大鼠在中央区运动距离和时间均减少.MWM结果显示,定位巡航期间,暴露组逃逸潜伏期时间增加,目标象限停留时间减少.空间探索期间,ACE-40组跨平台次数减少,目标象限内游泳速度降低.暴露组大鼠脑皮质和海马组织中MDA浓度增高;暴露组大鼠脑皮质SOD活性降低,海马组织SOD活性增高.Western Blot结果显示,与对照组相比,暴露组大鼠皮质和海马组织中IL-1β表达量增高;IL-10表达量降低.H&E结果显示,ACE-40组海马DG、CA3区神经元出现排列紊乱、层数减少和轮廓模糊.Nissl染色结果显示,暴露组大鼠海马DG、CA3区神经元数量减少,尼氏小体减少.以上结果表明,新生大鼠ACE亚慢性暴露能够导致成年后神经行为变化,可能与脑皮质和海马组织的氧化应激与炎症有关.

Aging is an important risk factor for neurodegenerative diseases. The activation of α7 nicotinic acetylcholine receptor (α7nAChR) is involved in inflammation and cognition, but the specific role it plays in aging remains unknown. This study aimed to investigate the anti-aging effect of the activation of α7nAChR on aging rats and BV2 cells induced by D-galactose, as well as its potential mechanism. D-galactose induced an increase in the SA-β-Gal positive cells, expression of p16 and p21 in vivo and in vitro. α7nAChR selective agonist PNU282987 decreased levels of pro-inflammatory factors, MDA, and Aβ, enhanced SOD activity and levels of anti-inflammatory factor (IL10) in vivo. PNU282987 enhanced the expression of Arg1, decreased the expression of iNOS, IL1β and TNFα in vitro. PNU282987 upregulated the levels of α7nAChR, Nrf2 and HO-1 in vivo and in vitro. The results of Morris water maze and novel object recognition tests showed that PNU282987 improved cognitive impairment in aging rats. Furthermore, α7nAChR selective inhibitor methyllycaconitine (MLA) results were opposite with PNU282987. PNU282987 improves cognitive impairment through inhibiting oxidative stress and neuroinflammation in D-galactose induced aging via regulating the α7nAChR/Nrf2/HO-1 signaling pathway. Therefore, targeting the α7nAChR may be a viable therapeutic approach for anti-inflammaging and neurodegenerative diseases.

目的 探讨不同年龄大鼠皮肤自然老化中的形态学变化规律及其机制.方法 取青年、中年、老年大鼠背部正中皮肤,采用形态学、分子生物学、体视学、电镜等技术观察增龄性皮肤组织中胶原纤维和弹力纤维,胶原原纤维的退化以及基质金属蛋白酶MMPs的相关变化.结果 随着年龄增长,皮肤含水量下降(P均<0.05),皮肤胶原蛋白、羟脯氨酸(HYP)含量呈年龄依赖性下降(P均<0.05).MMP1、MMP12的蛋白和mRNA表达水平随年龄增长递增(P均<0.05).时序性老化大鼠,表皮最薄,真皮萎缩明显,胶原纤维和弹力纤维含量最低(P均<0.05);超微结构观察,胶原原纤维直径小、间距小、横纹周期短(P均<0.05),密度最大(P<0.05).结论 表皮屏障受损,锁水能力下降,真皮基质金属蛋白酶MMPs激活,胶原纤维和弹力纤维退化,与时序性老化密切相关.

目的 观察大鼠生命早期抗生素暴露对其成年后肠-脑轴的影响.方法 选取出生后第21天的(PND21)雄性SD大鼠,随机分为对照组(Con)和抗生素组(Abx),日常饮用水分别给予无菌水和含有盐酸四环素(3周,2 g·L-1)、罗红霉素(1周,0.005 g·L-1)和盐酸环丙沙星(6周,0.1 g·L-1)的无菌水.第10周后采用Morris水迷宫实验观察SD大鼠认知行为变化;16SrDNA测序技术检测肠道菌群变化;ELISA法检测血清中肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-6、IL-1β 的水平;HE染色观察海马形态学改变.结果 与Con组相比,Abx组大鼠逃逸潜伏期延长(P<0.05);Abx组肠道菌群Chao1指数、Shannon指数和Simpson指数均降低(P均<0.01);在门水平上:Abx组厚壁菌门(Firmicutes)减少,疣微菌门(Verrucomicrobia)增多(P均<0.01);在属水平上:Abx组乳杆菌属(Lactobacillus)、Ruminococcaceae_UCG-005减少,艾克曼菌属(Akkermansia)、拟杆菌属(Bacteroides)增多(P均<0.01);Abx组大鼠血清中炎性因子TNF-α、IL-6、IL-1β水平均升高(P均<0.01);形态学观察发现Abx组大鼠海马齿状回闩区新生神经元疏松分布,排列不规则,细胞核固缩.结论 SD大鼠幼年抗生素慢性暴露,可引起成年后肠道菌群结构紊乱,成年后空间学习记忆能力减弱,破坏肠-脑轴功能稳态.

Type 2 diabetes mellitus (T2DM) is closely associated with chronic low-grade inflammation. Accumulating evidences suggest that GPR120 activation and NLRP3 inflammasome suppression contribute to ameliorate chronic inflammation. α-linolenic acid (ALA) has been proved to be beneficial in chronic metabolic diseases. However, the triggering mechanisms of ALA alleviated the inflammation in T2DM by GPR120-NLRP3 inflammasome pathway are still poorly understood. The present study was designed as two phase: in vivo, the levels of FBG, HbA1c, liver macrophages and NLRP3 inflammasome components were significantly attenuated with ALA intervention; in vitro, ALA inhibited the expression of NLRP3 inflammasome complex and the activation of NF-κB, enhanced GPR120 and subsequent β-arrestin2 in LPS-stimulated RAW264.7 cells. Intriguingly, blocked with GPR120 antagonist AH7614, the inhibitory effects of ALA on NLRP3 inflammasome and TLR4/NF-κB pathway activity were weakened. Collectively, these results indicated that ALA regulated macrophages by GPR120-NLRP3 pathway to ameliorate T2DM.

目的 研究回药复方丁香制剂联合布替萘芬治疗足癣的疗效并评估其安全性.方法 选取2019年1月～2020年1月接受诊疗的足癣患者97例为研究对象,按随机数表法分为A组(30例)、B组(32例)和C组(35例),对三组患者分别给予单纯布替萘芬治疗、单纯回药复方丁香制剂治疗和回药复方丁香制剂联合布替萘芬治疗,比较三组患者治疗前、治疗2周后、停药4周后临床症状评分、真菌镜检结果和疗效,并记录用药期间不良反应发生情况和持续时间.结果 治疗前、三组患者临床症状评分比较差异无统计学意义,治疗后C组临床症状评分低于A组和B组,且C组真菌清除率94.29％>B组90.62％>A组73.33％(P<0.05);停药4周后C组患者总有效率为97.14％>B组90.63％>A组76.67％(P<0.05);三组患者治疗期间不良反应发生率比较差异无统计学意义(P>0.05),C组患者不良反应持续时间少于A组和B组患者(P<0.05).结论 回药复方丁香制剂联合布替萘芬治疗足癣可取得显著疗效,对患者皮损、瘙痒等临床症状改善效果优于单纯布替萘芬或复方制剂治疗,且其对部分浅部癣菌具有较强的抑菌活性.

目的:对比研究128层螺旋C T冠状动脉血管成像与冠状动脉造影对冠心病诊断价值.方法:选取2016年1月—2019年1月我院疑似冠心病患者60例,所有病例均分别接受冠状动脉C T血管成像和冠状动脉造影检查,回顾性分析其临床资料,对比两种检查结果,以评估对冠心病诊断价值.结果:冠状动脉C T血管成像检出病变血管数为106支,检出率53％,冠状动脉造影检出病变血管数为94支,检出率47％;128层螺旋C T诊断冠心病敏感度89.9％,特异度90.3％,阳性预测值92.4％,阴性预测值97.6％,准确性91.7％,K A P P A值为42.8％.C A G检诊断冠心病的敏感度91.6％、特异度96.4％、阳性预测值94.0％和阴性预测值95.7％.结论:冠状动脉C T血管成像和冠状动脉造影对病变血管检出无明显差异,对冠状动脉轻中度狭窄判断准确率无明显差异,重度狭窄判断有一定差异性,但均无统计学意义,128排螺旋CT冠状动脉血管成像可以作为冠状动脉病变筛查的重要方法,对冠心病诊断具有一定应用价值.

目的:比较多模态MRI与CT动态增强两种检查方法对小肝癌的诊断效能.方法:选取2017年1月—2019年1月行肝脏CT及MRI检查并经病理证实的小肝癌患者45例,CT动态增强检查作为对照组,多模态磁共振成像检查作为观察组,比较两种方法检出肝内病灶数和小肝癌数,以病理为金标准对比两种检查方法对小肝癌的诊断准确率.结果:观察组的诊断准确率95％(23/24)显著高于对照组75％(18/24),(χ2=6.81,P<0.05);对比两组发现小肝癌个数,观察组显著多与对照组(t=3.18、3.25,P<0.05).结论:多模态磁共振成像检查对小肝癌的检出及诊断准确性较CT动态增强检查更高,更接近病理检查结果,值得临床应用.

为探讨"小组学习、问题导向"教学模式在留学生人体解剖学教学中的效果,选择宁夏医科大学6年制临床医学本科留学生,在人体解剖学教学中实施"小组学习、问题导向"教学模式.通过学生的出勤率、课堂讨论的参与度、课后作业的完成情况、标本考试、解剖操作等环节评价教学效果.结果发现"小组学习、问题导向"教学模式能极大调动学生的学习兴趣,夯实学生的解剖学基础知识,提高学生动手操作能力及应用解剖学知识分析临床相关问题的能力,并培养了学生的团队意识和协作精神,提高了教学质量.

目的 探讨癫痫患儿临床发作间期的瞬目反射变化特点.方法 选取癫痫患儿60例分成癫痫无智力低下组和癫痫伴智力低下组,同时选取年龄相当的同期健康儿童60例为对照组,在临床发作间歇期进行瞬目反射(BR)检测.结果 癫痫组患儿瞬目反射的异常率高于对照组(P＜0.05);癫痫伴智力低下组BR异常率明显高于癫痫无智力低下组(P＜0.05).癫痫伴智力低下组及癫痫无智力低下组与对照组比较BR的R2、R2'波潜伏期均延长(P＜0.05).癫痫伴智力低下组与癫痫无智力低下组比较,BR的R2、RR2'波潜伏期显著延长(P＜0.05).结论 癫痫患儿BR异常率高,癫痫伴智力低下者BR变化更为显著,其主要特征为R2、R2'波潜伏期延长.结果提示癫痫儿童存在脑干功能的损害,脑干功能的损害在癫痫伴智力低下的儿童中更为明显.

目的 评价认知功能刺激疗法(CST)对轻度认知功能损害(MCI)患者的影响.方法 对20例试验对象运用CST方法 进行干预训练,训练内容为智力训练、定向力训练、语言及记忆能力训练、生活能力训练等,通过一般生活质量变化、简易精神状态检查量表(MMSE)、日常生活能力评定量表(ADL)、蒙特利尔认知评估量表(MoCA)进行评定.结果 经过4周的干预训练后,MCI患者的MMSE和MoCA评分与干预前的差异具有统计学意义(P<0.05).结论 MCI患者经过认知功能训练可延缓痴呆的进展,是目前有效治疗方法 之一.

为观察新生鼠全氟辛烷磺酸(PFOS)低剂量慢暴露对其成年后神经行为和海马组织影响,选取出生后5-7 d雄性SD幼鼠80只,按体重随机分为4组,分别为对照组(Con)、低剂量组(P5)、中剂量组(P10)、高剂量组(P20),每组各20只.从PND7开始染毒,共染毒12周,动态记录体重,并进行水迷宫、旷场实验、滚轮实验观察神经行为变化,同时取材进行HE染色,观察海马形态学改变.结果显示与Con组比较,P20组染毒8d后出现体重增长减缓(P＜0.05),4周时P10和P20组死亡率明显升高;并且P10、P20组在4周,P5组在8周时,水迷宫实验逃逸潜伏期延长,目标象限停留时间缩短;P10、P20组大鼠在4周,P5组在8周时,旷场实验中央格停留时间延长,站立次数减少,行走总距离缩短;滚轮试验中,对照组和P5组肢体运动协调能力无显著性差异.P5组在染毒12周时出现海马神经元排列紊乱,胞核固缩及胞体胀大,CA1区细胞和齿状回闩区神经前体细胞数量明显少于Con组(P＜0.01).上述结果表明,大鼠幼年PFOS低剂量慢暴露可损害其成年后空间学习记忆及自主探究能力,这种损害可能与海马神经元发生不足有关.