BACKGROUND:Neuroinflammation is a critical aspect of aging and neurodegenerative disorders, increasingly recognized for its significant role in the progression of cognitive impairments. Mitochondrial homeostasis is closely linked to cognitive function in the aging brain. However, it remains unclear whether exercise can safeguard cognitive function by enhancing mitochondrial homeostasis in the aged hippocampus affected by neuroinflammation. METHODS:In this study, we established mouse models exhibiting memory impairment and neuroinflammation in the aged hippocampus to investigate whether exercise can reverse lipopolysaccharides (LPS)-induced cognitive dysfunction in aged mice, reduce neuroinflammation, and simultaneously improve mitochondrial homeostasis in the hippocampus. Eighteen-month-old male ICR mice underwent 8 weeks of moderate-intensity aerobic exercise. RESULTS:The exercise regimen enhanced memory function in LPS-injected aged mice, which was accompanied by reductions in inflammation, oxidative stress, and apoptosis in the aged hippocampus. Importantly, exercise improved mitochondrial homeostasis in the hippocampus of LPS-injected aged mice. CONCLUSION:our results provide the first evidence that exercise can protect cognitive function in the context of neuroinflammation in the aged hippocampus, suggesting that this effect may be associated with the improvement of mitochondrial homeostasis.

Growing evidence suggests that exercise can provide neuroprotection by improving mitochondrial quality control (MQC) on the aged brain. Adenosine 5 '-monophosphate (AMP)-activated protein kinase (AMPK) signaling responsiveness declines with aging. However, whether AMPK plays a role in the exercise-mediated improvement of memory and MQC in the aged hippocampus remains to be established. 5-Aminoimidazole 4-carboxamide ribonucleoside (AICAR), a pharmacological agonist of AMPK, has been proposed to be an exercise mimetic recently. However, it has not been clarifi ed whether AICAR could mimic the eff ects of exercise on the aged hippocampus through improvement of MQC. In this study, AICAR (AMPK agonist) and Compound C (AMPK inhibitor) were used to investigate if AMPK plays a key role in exercise-induced improvement of MQC and if AICAR could act as an exercise mimetic through improvement of MQC in aged hippocampus. Both exercise and AICAR improved the memory of aged mice and increased AMPK phosphorylation in the aged hippocampus. Exercise, but not AICAR, improved mitochondrial respiratory function in the aged hippocampus and increased the microtubule associated protein 1 light chain 3 (LC3)-II/LC3-I ratio and the protein expression of LC3-II and autophagy related protein 7 (ATG7) in the lysate of whole hippocampal tissue. Both exercise and AICAR increased the ratio of LC3-II/LC3-I and the protein expression of LC3-II in the mitochondrial fractions of the hippocampus. Regarding mitochondrial dynamics, neither exercise training nor AICAR changed the protein level of mitofusin 2 (Mfn2). Exercise, but not AICAR, increased the protein level of dynamin-related protein 1 (Drp1). Furthermore, both exercise training and AICAR increased the protein level of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1 alpha), a modulator of mitochondrial biogenesis. Compound C abolished the exercise-induced effects on memory in aged mice, AMPK phosphorylation, autophagy, mitophagy, and mitochondrial fi ssion in the aged hippocampus. However, Compound C did not reverse the exercise-induced increase in PGC-1 alpha protein levels in the aged hippocampus. Our data provide evidence that AMPK plays an important role in the exercise-induced improvement of memory and MQC in the hippocampus of aged mice. Importantly, we demonstrated for the fi rst time that AICAR could partially mimetic the benefi cial eff ects of endurance exercise on memory and MQC in the hippocampus of aged mice, and thus may be a promising exercise mimetic for counteracting brain aging.

ObjectiveThe Mediterranean diet (MD), a widely recognized healthy dietary pattern, has demonstrated significant value in the prevention and management of metabolic syndrome (MetS). However, quantitative integrated analyses of its mechanisms of action remain scarce, highlighting an urgent need for systematic collation.MethodsThis study retrieved relevant literature published between 2015 and 2025 from the Web of Science and Scopus databases, and conducted visual bibliometric analyses using R software (Bibliometrix package), VOSviewer, and CiteSpace.ResultsA total of 1723 valid articles were identified from the Web of Science, and 1061 from Scopus. The number of publications steadily increased from 2015 to 2022, with a particularly notable growth spurt between 2016 and 2018, followed by a slight decline from 2022 to 2024. Spain led significantly in the number of publications, followed by Italy, the United States, and Iran, and Spain has established an extensive international cooperation network. At the journal level, Nutrients serves as the core academic platform in this field, ranking first in both publication volume and citation frequency. Current research hotspots primarily focus on the regulatory effects of MD on blood glucose homeostasis, insulin sensitivity, lipid metabolism, and blood pressure in MetS patients, as well as the mechanisms by which bioactive components (e.g., polyphenols, unsaturated fatty acids, and vitamins) promote metabolic health through anti-inflammatory, antioxidant, and insulin-sensitizing pathways. Gut microbiota modulation has evolved into an emerging research direction in this domain.ConclusionOver the past decade, interdisciplinary research on MD and MetS has gained increasing attention and is expected to become a core focus in the non-pharmacological intervention of MetS. This study systematically clarifies the research status, hot topics, and developmental context of this field, providing important references for future precision nutrition mechanism research and clinical intervention trials.

Background Dysregulation of mitochondrial dynamics, including fusion/fission, transport, mitophagy and biogenesis, plays a crucial role in neurodegenerative diseases. However, a systematic quantitative mapping of the knowledge structure (i.e., key research themes, foundational references, and citation/collaboration clusters) and evolving research trends (i.e., research hotspots over time) in this research field is lacking. Methods Empirical and review article on mitochondrial dynamics in neurodegenerative diseases, which published in English from 2005 to 2025, were retrieved from the Web of Science Core Collection and Scopus. BibliometriX, VOSviewer, and CiteSpace were applied to perform the bibliometric analysis and science mapping. Scientific performance analyses, collaborative networks of authors/institutions/countries, reference co-citation networks, keyword bursts analysis were conducted. Results A total of 834 documents were included, revealing a rapid growth in scientific productivity from 2005 to 2025. The United States, China, and Germany were the most productive countries, with institutions such as Case Western Reserve University and Texas Tech University serving as major hubs. Co-citation and keyword burst analyses reveal a distinct temporal shift: from foundational studies of fusion/fission machinery and oxidative stress toward an integrated Mitochondrial Quality Control paradigm encompassing mitophagy, dynamics, and biogenesis. Key emerging hotspots include mitochondrial biogenesis, mitochondrial transport, and quality control mechanisms. Translational frontiers prioritize enhancing PINK1/Parkin-mediated mitophagy, inhibiting Drp1-driven excessive fission, and activating PGC-1α-dependent biogenesis. Conclusion This bibliometric study maps the intellectual structure and evolutionary trajectory of mitochondrial dynamics research in neurodegenerative diseases. It documents a field-wide paradigm shift toward a translational agenda centered on the MQC framework. Furthermore, the findings highlight the necessity of integrating pharmacological interventions with lifestyle modifications and precision medicine approaches to overcome translational barriers and develop effective disease-modifying strategies.

Ischemic stroke (IS) continues to be a major contributor to global mortality and long - term disability. Buyang Huanwu Decoction (BHD), a traditional Chinese medicine formula, has shown effectiveness in reducing brain injury and promoting post - stroke recovery through experimental researches and clinical trials. The neuroprotective mechanisms of BHD against cerebral ischemic injury involve multiple pathways, such as suppression of inflammation, reduction of oxidative stress, inhibition of apoptosis, regulation of autophagy, and enhancement of mitochondrial function. Moreover, BHD presents therapeutic potential by boosting neuroplasticity, enhancing angiogenesis, reducing excitotoxicity, optimizing brain energy metabolism, and regulating gut microbiota. Considering the current scarce effective treatments for IS, exploring BHD’s therapeutic potential and its mechanism holds substantial clinical significance. This review systematically organizes recent research advancements on BHD’s application in IS management and its underlying mechanisms, providing useful insights for future research and clinical practice.

Nicotinamide adenine dinucleotide (NAD+) is a crucial coenzyme involved in catalyzing cellular redox reactions and serving as a substrate for NAD+-dependent enzymes. It plays a vital role in maintaining tissue homeostasis and promoting healthy aging. Exercise, a well-established and cost-effective method for enhancing health, can influence various pathways related to NAD+ metabolism. Strategies such as supplementing NAD+ precursors, modulating NAD+ synthesis enzymes, or inhibiting enzymes that consume NAD+ can help restore NAD+ balance and improve exercise performance. Various overlapping signaling pathways are known to play a crucial role in the beneficial effects of both NAD+ and exercise on enhancing health and slowing aging process. Studies indicate that a combined strategy of exercise and NAD+ supplementation could synergistically enhance athletic capacity. This review provides an overview of current research on the interactions between exercise and the NAD+ network, underscoring the significance of NAD+ homeostasis in exercise performance. It also offers insights into enhancing exercise capacity and improving aging-related diseases through the optimal use of exercise interventions and NAD+ supplementation methods.

Obesity impairs the health and regeneration of skeletal muscle. Astaxanthin (AX) possesses antioxidant and anti-obesity properties, making it possible to improve obesity-associated damages. 42 male C57BL/6J mice were fed a control diet, a high-fat diet (HFD) or a HFD with 0.02 %AX for 16 weeks. Mice were either immediately euthanized (experiment one) or given intramuscular injections of cardiotoxin (CTX) and euthanized on the seventh day (experiment two). The experiment one showed that AX improved grip strength and motor function with reduced fat deposition and elevated SOD in skeletal muscle. The experiment two found that AX increased the expression of proteins related to muscle regeneration and mitochondrial biogenesis. The in vitro experiment of interfering C2C12 myogenic cells with AX suggested that AX promoted myoblast differentiation and mitochondrial biogenesis. In conclusion, astaxanthin improves skeletal muscle health and regeneration in obese mice induced by HFD.

Exercise is known to be an effective intervention for depression. NADPH has been demonstrated to have neuroprotective effects in our previous studies. This study aimed to investigate if NADPH has antidepressant effects and can mimic the effects of exercise in a chronic unpredictable stress (CUS) rat model. CUS rats underwent an 8week swimming exercise (30 min/d, 5d/w) or were intraperitoneally administered 4 mg/kg or 8 mg/kg NADPH. The open field test (OFT), sucrose preference test (SPT), novelty-suppressed feeding test (NSFT), and forced swimming test (FST) were used to examine the antidepressant-like behaviors of the rats. Exercise, 4 mg/kg, and 8 mg/kg NADPH similarly reduced anxiety, as demonstrated by the number of fecal pellets. Meanwhile, exercise and 8 mg/kg NADPH significantly increased locomotion activity in the OFT. Exercise, 4 mg/kg, and 8 mg/kg NADPH effectively reversed CUS-induced anhedonia in rats in the SPT. Exercise, 4 mg/kg, and 8 mg/kg NADPH had no impact on appetite of depressed rats; however, 8 mg/kg NADPH increased the rats' exploratory activity in the NSFT. Exercise, 4 mg/kg, and 8 mg/kg NADPH significantly reduced the immobility time of CUS model rats, while exercise and 8 mg/kg NADPH postponed the early CUS-induced "immobility" in the FST. These results demonstrated that NADPH has similar antidepressant-like effects to exercise in CUS-induced depression model rats and is a potential exercise-mimicking antidepressant.

Lung adenocarcinoma is a highly aggressive subtype of lung cancer with a high mortality rate, which makes the investigation of novel lung adenocarcinoma therapeutic targets essential. Since oxidative stress has been shown to be a cancer-specific deplete in the lung, which is highly associated with oxidative stress, it is crucial to investigate and assess the clinical value of oxidative stress-related target genes in lung adenocarcinoma. In the current study, we obtained 3170 differentially expressed genes via differential analysis and 1058 oxidative stress-related genes via the molecular signatures database. Upon analyzing their intersection, 207 genes were identified. tRNA-histidine guanylyltransferase 1 like protein, glutathione peroxidase 8, and mitogen-activated protein kinase 3 were identified as lung adenocarcinoma biomarkers using machine learning algorithms. The tumor immune infiltrating analysis revealed that the tRNA-histidine guanylyltransferase 1 like protein gene is associated with the infiltration of regulatory T cells. In addition, the multivariate analysis revealed that elevated tRNA-histidine guanylyltransferase 1 like protein expression is a significant, independent predictor of overall survival. Furthermore, the pan-cancer analysis revealed that elevated tRNA-histidine guanylyltransferase 1 like protein expression is related to a worse prognosis in a variety of cancers. In light of these findings, the identification of tRNA-histidine guanylyltransferase 1 like protein as a novel biological marker may shed light on potential function mechanisms and the impact of the immune microenvironment in lung adenocarcinoma.

Evidence from clinical studies and preclinical studies supports that exercise preconditioning can not only reduce the risk of stroke but also improve brain tissue and functional outcome after stroke. It has been demonstrated that autophagy and mitochondrial dynamics are involved in ischemic stroke. However, it is still unclear whether exercise preconditioning-induced neuroprotection against stroke is associated with modulation of autophagy and mitochondrial dynamics. Although age and sex interactively affect ischemic stroke risk, incidence, and outcome, studies based on young male animals are most often used to explore the role of exercise preconditioning in the prevention of ischemic stroke. In the current study, we examined whether exercise preconditioning could modulate autophagy and mitochondrial dynamics in a brain ischemia and reperfusion (I/R) model of female aged mice. The results showed that exercise preconditioning reduced infarct volume and improved neurological deficits. Additionally, increased levels of autophagy-related proteins LC3-II/LC3-I, LC3-II, p62, Atg7, and mitophagy-related proteins Bnip3L and Parkin, as well as increased levels of mitochondrial fusion modulator Mfn2 and mitochondrial fission modulator Drp1 in the ischemic cortex of female aged mice at 12 h after I/R were present. Our results could contribute to a better understanding of exercise preconditioning-induced neuroprotection against ischemic stroke for the elderly.

BACKGROUND:Mitochondrial autophagy, the elimination of damaged mitochondria through autophagy, contributes to neuron survival in cerebral ischemia. Long non-coding RNAs (lncRNAs)/microRNAs (miRNAs)/mRNAs are important regulatory networks implicated in various biological processes, including cerebral ischemia-reperfusion (I/R) injury. Therefore, this work clarifies a novel RGD1564534-mediated regulatory network on mitochondrial autophagy in cerebral I/R injury.METHODS:Differentially expressed lncRNAs in cerebral I/R injury were predicted by bioinformatics analysis. Expression of RGD1564534 was examined in the established middle cerebral artery occlusion (MCAO) rats and oxygen glucose deprivation/reoxygenation (OGD/R)-exposed neurons. We conducted luciferase activity, RNA pull-down and RIP assays to illustrate the interaction among RGD1564534, miR-101a-3p and Dusp1. Gain- or loss-of-function approaches were used to manipulate RGD1564534 and Dusp1 expression. The mechanism of RGD1564534 in cerebral I/R injury was evaluated both in vivo and in vitro.RESULTS:RGD1564534 was poorly expressed in the MCAO rats and OGD/R-treated cells, while its high expression attenuated nerve damage, cognitive dysfunction, brain white matter and small vessel damage in MCAO rats. In addition, RGD1564534 promoted mitochondrial autophagy and inhibited NLRP3 inflammasome activity. RGD1564534 competitively bound to miR-101a-3p and attenuated its binding to Dusp1, increasing the expression of Dusp1 in neurons. By this mechanism, RGD1564534 enhanced mitochondrial autophagy, reduced NLRP3 inflammasome activity and suppressed the neuron apoptosis induced by OGD/R.CONCLUSION:Altogether, RGD1564534 elevates the expression of Dusp1 by competitively binding to miR-101a-3p, which facilitates mitochondrial autophagy-mediated inactivation of NLRP3 inflammasome and thus retards cerebral I/R injury.

放射性肺损伤(RILI)是肺癌、食管癌等胸部肿瘤放射治疗引起的常见且较为严重的不良反应,包括早期的急性放射性肺炎和晚期的放射性肺纤维化.由于肺组织对放射线较为敏感,当其接受一定放射剂量时可能发生RILI.中药对于RILI具有一定防治作用,从现代医学角度探索其防治机制涉及细胞因子学说、细胞损伤学说及免疫学说.下一步期待对放射性肺损伤的发生机制做更深入地研究,也能通过实验研究从肺纤维化相关通路与差异代谢物方面进一步明确中药防治放射性肺损伤的作用机制,更好地为临床提供指导.

放射性食管炎是颈胸部恶性肿瘤放疗期间发生的常见不良反应.在"瘀热"理论的指导下,吴勉华教授提出该病核心病机为瘀热蕴结、管络损伤、气阴两伤,倡导以凉血化瘀、和胃护络、益气养阴为主要治疗大法,并自拟"益和启膈饮"化裁治疗本病,疗效显著.附验案1则以佐证.

目的 通过对温病学派医著的整理,分析温病学派医家使用鲜药的方法和规律.方法 整理使用鲜药的医案、处方,对鲜药的名称、病证范围、使用频数、性味、归经、用法用量等信息进行统计分析.结果 医案中使用鲜药的病案共1 748例,主治以风温病、疟疾、血证为主,鲜药品种182种,使用频次2974次.鲜药性味甘、寒,主入上中焦,归胃、肺经,多数药物使用剂量较大,并有其特殊的服用方法.结论 鲜药因清润的特质在温病治疗中应用广泛,其特殊的用法用量值得关注.

目的:通过分析消化内科患者入院时药物重整情况,为临床药师参与消化内科患者入院时药物管理及用药指导提供参考.方法:选择2019年6月至2020年6月某院消化内科新入院患者,纳入入院前存在服用药物的病例,通过药学问诊,记录患者的用药目的、用法用量、慢病是否定期随访或监测指标值、过敏史.结果:共纳入111例病例,其中有慢病史的102例,占比91.89％;平均服用药物数量为4.04种;平均药疗差异问题数为1.81;存在药疗差异的有92例,占比82.88％,其中接受药师建议的有90例,占比97.83％.结论:患者自我药疗偏差较大,部分患者规范就医用药意识薄弱;临床药师可通过入院时的药学问诊以及用药宣教提高患者用药的安全性和有效性.

A 43-year-old female patient received Fuyanshu capsules 1.6 g orally thrice daily for pelvic inflammation. The traditional Chinese medicine decoction was added 1 week later. After 10 days of combination therapy, the patient developed fatigue, which was gradually aggravated, and yellowish skin and sclera appeared. Seven days later, laboratory tests showed alanine aminotransferase (ALT) >1 000 U/L, aspartate aminotransferase (AST) >750 U/L, gamma-glutamyltransferase (γ-GT) 148 U/L, alkaline phosphatase (ALP) 153 U/L, and total bilirubin (TBil) 56.3 μmol//L. After excluding viral hepatitis, autoimmune liver disease, obstructive jaundice, and other causes, liver injury caused by Fuyanshu capsules combined with traditional Chinese medicine decoction was considered. After Fuyanshu capsules and traditional Chinese medicine decoction were discontinued, reduced glutathione, glycyrrhizic acid preparation, and ursodeoxycholic acid were given. Seven days later, the patient′s symptoms were improved obviously and laboratory tests showed ALT 323 U/L, AST 125 U/L, γ-GT 149 U/L, ALP 109 U/L, and TBil 35.8 μmol/L. Twenty-seven days later, the patient′s symptoms disappeared and laboratory tests showed ALT 62 U/L, AST 42 U/L, γ-GT 67 U/L, ALP 67 U/L, and TBil 18.7 μmol/L. There are 7 same components in Fuyanshu capsule and traditional Chinese medicine decoction. It was considered that the liver injury was related to the increase of hepatotoxicity caused by the combination of the two drugs.

目的:分析医院静脉用药调配中心(PIVAS)医嘱用药的合理性以及不合理的原因.方法:抽取2019年PIVAS接收的静脉用药医嘱107 541份,应用Excel 2003版统计学软件分析其用药的合理性并找出不合理的原因及解决措施.结果:107 541份用药医嘱中,审核出1 236份不合理医嘱,其用药的不合理率为1.15％;不合理用药涉及的主要科室有普外科、风湿科、肿瘤内科,不合理用药原因涉及间隔液、给药剂量、给药频次、溶媒选择、配伍禁忌等,其中1 042份医嘱做出修改,其医嘱的修改率为84.30％.结论:PIVAS药师通过审核临床各病区提交的用药医嘱,能及时发现医嘱用药的不合理性,并及时与临床相关人员沟通,有效降低了住院患者静脉用药医嘱的不合理率,体现处方前置审核的意义,确保了患者安全合理用药.

目的 探讨胃癌气阴两虚证患者舌苔菌群变化的炎症代谢机制.方法 基于医院开展病例-对照研究,纳入13例胃癌气阴两虚证患者,以23例健康人为对照组,高通量测序分析舌苔菌群,电化学发光技术检测血清20种炎症因子,气相色谱质谱联用检测血清代谢组学.结果 与对照组相比,胃癌气阴两虚证患者舌苔细菌Shannon指数降低(P<0.05),而舌苔真菌Alpha多样性差异无统计学意义(P>0.05).判别分析显示,舌苔的3个细菌属(柄细菌属、巨单胞菌属、木洞菌属)和1个真菌属(裂壳属)是胃癌气阴两虚证的标志菌群.胃癌气阴两虚证患者血清谷氨酸、L-组氨酸、肌酸等15种代谢分子水平升高(P<0.05),IL-17α、TNF-α、IL-6等8种血清炎症因子水平升高(P<0.05).相关性分析发现,IL-17α、IL-6、TNF-α与梭杆菌属、卟啉单胞菌属显著负相关(r<-0.4,P<0.05),梭杆菌属、消化链球菌属与血清谷氨酸代谢水平显著负相关(r<-0.4,P<0.05).结论 胃癌气阴两虚证患者舌苔菌群与血清炎症因子、代谢分子相关,为阐明气阴两虚证的形成机制提供了新的切入点.