RENAL FAILURE
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2026
·
IF 3.8
Zhuangzhi Yang,Xiaowei Zhou,Chenhao Wu,Xia Lin
Objectives: Nicotiflorin has demonstrated efficacy in mitigating acute liver injury, and therefore, its potential in treating septic acute kidney injury (AKI) merits further investigation. This study evaluated whether nicotiflorin restores mitochondrial function and reduces oxidative stress in septic AKI via mediating the PTEN-induced putative protein kinase 1 (PINK1)/Parkin signaling pathway.Methods: Lipopolysaccharide (LPS) was applied to replicate septic AKI in C57BL/6 mice and NRK-52E cells, which were later treated with nicotiflorin. Renal function was assessed through biochemical markers, histopathology, and immunofluorescence. The impact of nicotiflorin on cell viability, apoptosis, and mitochondrial function was analyzed using cell counting kit 8 assay and flow cytometry. Mtphagy and Lyso staining was utilized to evaluate the effect of nicotiflorin on mitophagy in LPS-induced cells. Molecularly, Western blot was employed to quantify protein expressions of genes related to apoptosis, mitophagy and oxidative stress in vivo and in vitro.Results: Nicotiflorin treatment significantly improved renal dysfunction, kidney damage, reduced levels of apoptosis-related proteins, increased expressions of PINK1, Parkin, and LC3II/LC3I, and decreased expression of p62 in LPS-induced mice. In NRK-52E cells, nicotiflorin abrogated LPS-triggered reduction in cell viability, increase in apoptosis, elevation in ROS and mitochondrial mass, reduction in mitochondrial membrane potential, upregulation of apoptotic proteins, downregulated NF-E2-related factor-2 (Nrf2), PINK1, Parkin and LC3II/LC3I, and increased expressions of kelch-like ECH-associated protein 1 (KEAP1) and p62.Conclusions: Nicotiflorin attenuates mitochondrial dysfunction and oxidative stress in septic AKI via PINK1/Parkin signaling pathway, suggesting its potential as a therapeutic agent for septic AKI.
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IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY
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2023
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IF 3.3
Yuxuan Chen,Wei Cao,Bin Li,Xiaofei Qiao,Xiangdong Wang,Guang Yang,Siying Li
Objective: Sepsis is one of major reasons of cardiorenal syndrome type 5 (CRS-5), resulting in irreversible tissue damage and organ dysfunction. Macrophage has been demonstrated to play key role in the pathophysiology of sepsis, highlighting the need to identify therapeutic targets for modulating macrophage phenotype in sepsis.Methods and Results: In this study, a rapid-releasing hydrogen sulfide (H2S) donor NaSH, and a slow-releasing H2S compound S-propargyl-cysteine (SPRC) which is derived from garlic, have been studied for the immune-regulatory effects on macrophages. The NaSH and SPRC showed the potential to protect the heart and kidney from tissue injury induced by LPS. The immunohistochemistry of F4/80+ revealed that the infiltration of macrophages in the heart and kidney tissues of LPS-treated mice was reduced by NaSH and SPRC. In addition, in the LPS-triggered inflammatory cascade of RAW264.7 macrophage cells, NaSH and SPRC exhibited significantly inhibitory effects on the secretion of inflammatory cytokines, production of reactive oxygen species (ROS), and regulation of the macrophage phenotype from M1-like to M2-like. Moreover, autophagy, a crucial process involved in the elimination of impaired proteins and organelles during oxidative stress and immune response, was induced by NaSH and SPRC in the presence of LPS stimulation. Consequently, there was an increase in the number of mitochondria and an improvement in mitochondrial membrane potential. This process was mainly mediated by PINK1/Parkin pathway mediated mitophagy.Discussion: These results demonstrated that the immunoregulatory effects of H2S donors were through the PINK1/Parkin-mediated mitophagy pathway. Overall, our study provided a new therapeutic direction in LPS-induced cardiorenal injury.
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JOURNAL OF ENVIRONMENTAL SCIENCE AND HEALTH PART A-TOXIC/HAZARDOUS SUBSTANCES & ENVIRONMENTAL ENGINEERING
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2026
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IF 2
Jing Zhu,Mengmeng Gao,Hao Ling,Phar Ku Ngwe,Chengxiang Guo,Yinan Hu,Jicang Wang
This study investigated the protective effects of naringenin (Nar) against lead (Pb)-induced testicular injury in rats, focusing on the Nrf2/Keap1 antioxidant pathway and PINK1/Parkin-mediated mitophagy. To this end, male SD rats were exposed to Pb (60 mg/kg) and co-treated with Nar (50 mg/kg) for 8 consecutive weeks, followed by assessments via biochemical detection, oxidative stress (OS) evaluation, hematological examination, histopathological observation, qPCR, WB, and IHC analyses. Pb exposure caused hematological disturbances, reduced serum LH and T levels, and OS imbalance (lower GSH, SOD, CAT; higher MDA), aggravating testicular damage. Meanwhile, it suppressed the Nrf2/NQO1 pathway, elevated Keap1, impaired autophagy (elevated p62, declined LC3‑II/LC3‑I ratio), and induced aberrant accumulation of PINK1/Parkin. Co-treatment with Nar mitigated these alterations, ameliorating testicular injury, restoring redox homeostasis and serum reproductive hormone levels, and normalizing key molecular expressions in both pathways. In conclusion, Nar alleviates Pb-induced rat testicular damage by reactivating the Nrf2/Keap1 axis to suppress OS, and by restoring autophagic flux to facilitate PINK1/Parkin-mediated clearance of damaged mitochondria.
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PHYTOTHERAPY RESEARCH
·
2026
·
IF 8.1
Shuanggong Liu,Jie Zhao,Shuhang Dong,Yang Zhang,Yachao Zhao,Ning Ran,Guowei Yang,Changliang Peng,Xu Yang,Guangxu Song,Yingze Zhang,Dongjin Wu
Intervertebral disc degeneration (IVDD) is a major cause of chronic low back pain and is driven by oxidative stress, inflammation, and ferroptosis. While mitophagy regulates ferroptosis in other diseases, its role in IVDD remains unclear. The potential of scutellarein, a flavonoid with antioxidant properties, to treat IVDD has not yet been explored. Primary human nucleus pulposus (HNP) cells were treated with tert-butyl hydroperoxide (TBHP) to establish an in vitro IVDD model. Mitophagy was inhibited by cyclosporin A (CsA) treatment. Radiographic and histopathological analyses were performed in a rodent IVDD model. Key markers (IL-1β, ACSL4, GPX4, PINK1, LC3, and PI3K/mTOR) were assessed. Scutellarein preserved the NPC phenotype, reduced inflammation, and suppressed ferroptosis by activating PINK1/Parkin-mediated mitophagy. It restored mitochondrial function and inhibited the PI3K/AKT/mTOR pathway. In vivo, scutellarein attenuated IVDD progression; downregulated the expression of IL-1β and ACSL4; and upregulated the expression of collagen II, GPX4, PINK1, and LC3. Scutellarein mitigates IVDD by inducing mitophagy to inhibit ferroptosis and restore mitochondrial function, highlighting its therapeutic potential.
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BRAIN RESEARCH BULLETIN
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2026
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IF 4.5
Feifei Chen,Lingkai Tang,Ling Yuan,Jiali Xiong,Rong Kuang,Wen Qian,Yufang Kong,Yina Yin
UB alleviates CUMS-induced depressive-like behaviors and hippocampal damage in rats. • The antidepressant effect of UB may be associated with the upregulation of SLP2 expression in hippocampal neurons of rats. • SLP2 regulates the PINK1/Parkin pathway, promotes mitophagy, and maintains neuronal energy homeostasis. • Knockdown of SLP2 in vivo reverses the antidepressant and neuroprotective effects of UB. Background Depression is a highly prevalent mental disorder, with current medications often limited by delayed onset and insufficient efficacy, underscoring the urgent need to explore novel therapeutic strategies. Urolithin B (UB), a natural ellagitannin-derived metabolite, exhibits anti-inflammatory and antioxidant activities in neuroinflammation, yet its role in depression remains unclear. Objective: The present research aimed to uncover possible effects of UB on depressive-like behavior and hippocampal neuronal damage in a rat model of depression and to preliminarily elucidate its underlying molecular mechanisms. Methods: A rat model of depression was created using the chronic unpredictable mild stress (CUMS) paradigm, after which UB intervention was applied. To evaluate depressive-like behaviors, several behavioral tests were conducted, including sucrose preference test, forced swim test, tail suspension test, and open field test. Hippocampal pathological changes and related factor expression were evaluated using histopathology, immunofluorescence, and ELISA. Potential targets were screened via single-cell RNA sequencing (scRNA-seq) data obtained from the GEO database. Subsequently, the function of the identified target gene was validated through in vitro knockdown/overexpression experiments and an in vivo rescue experiment. Results: UB significantly ameliorated depressive-like behaviors in CUMS rats and alleviated hippocampal neuronal damage, synaptic loss, and neuroinflammation. scRNA-seq analysis revealed a significant upregulation of SLP2 expression in hippocampal neurons (HNs) from the treated group, along with the enrichment of mitophagy-related pathways. Functional experiments confirmed that SLP2 regulates the PINK1/Parkin pathway, promotes mitophagy, and maintains neuronal energy homeostasis. Conversely, knockdown of SLP2 reversed the antidepressant and neuroprotective effects of UB. Conclusion: UB alleviates CUMS-induced depressive-like behavior and hippocampal neuronal damage by upregulating SLP2 and regulating the PINK1/Parkin-mediated mitophagy pathway. This study presents a new potential target and theoretical basis for developing natural compound-based therapies for depression.
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JOURNAL OF ETHNOPHARMACOLOGY
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2026
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IF 5.4
Jinni Meng,Ping Wei,Heping Yang,Lin Chen,Cheng Peng,Ou Dai,Qinmei Zhou,Liang Xiong
Ethnopharmacological relevance Ligusticum chuanxiong Hort. (Chuanxiong) is a traditional Chinese medicinal herb whose rhizome has been historically and clinically used to treat conditions such as headache, dizziness, and depression. These traditional application broadly correlate with modern diagnoses of cerebrovascular dysfunction, impaired cerebral blood flow, and neuroinflammation. As a characteristic phthalide dimer and major bioactive constituent of Chuanxiong, levistilide A (LA) has shown significant therapeutic potential. However, its specific antidepressant and anxiolytic properties require further clarification. Aim of the study This study aimed to assess the efficacy of LA against depression and anxiety, with the further goal of elucidating its underlying molecular mechanisms. Materials and methods A depression- and anxiety-like state was induced in C57BL/6 mice by LPS challenge after which they received therapeutic intervention with different doses of LA. The therapeutic efficacy was assessed by behavioral tests, histopathological analyses, and enzyme-linked immunosorbent assays (ELISA). Concurrently, we assessed microglial activation via immunofluorescence, along with mitochondrial status by measuring reactive oxygen species (ROS) levels with flow cytometry and examining ultrastructure with transmission electron microscopy (TEM). To investigate the cellular mechanisms, LPS-stimulated BV2 cells was established . In this model, autophagic flux was quantitatively measured using Bafilomycin A1 (Baf A1) inhibition assays combined with western blot analysis of LC3B-II. And mitophagy was evaluated by co-immunofluorescence LC3B with the mitochondrial marker Tomm40 in both BV2 cells and mouse hippocampal CA3. Building on this, computational approaches, along with experimental methodologies including immunofluorescence and western blotting, were utilized to elucidate the underlying molecular mechanisms. Furthermore, SIRT3-specific siRNA ( siRNA -SIRT3) was used for further validation. Results The LA treatment demonstrated a notable protective role against LPS-induced depression and anxiety through ameliorating behaviors accompanied by depression- and anxiety-like behaviors, attenuating neuronal damage, downregulating pro-inflammatory cytokine expression levels, and suppressing microglial overactivation. Mechanistically, LA alleviated oxidative stress and mitochondrial dysfunction by reducing ROS accumulation and mitigating mitochondrial damage. In the LPS-induced BV2 cells, LA treatment significantly enhanced autophagic flux, as evidenced by the further accumulation of LC3B-II upon Baf A1 inhibition, which confirmed the promotion of functional autophagy. Concurrently, the increased co-localization of Tomm40 with LC3B upon LA treatment provided direct evidence for mitophagy activation. Molecular docking combined with molecular dynamics simulation analyses revealed robust binding interactions between LA and SIRT3, as well as between SIRT3 and PINK1. Further investigation into the downstream pathway revealed that LA effectively activated the SIRT3/PINK1/Parkin pathway. This was supported by the western blot analyses. Specifically, LA treatment increased the SIRT3, PINK1, Parkin, and LC3B-II expression levels, while it decreased p62 levels. This result suggested mitophagy activation. An immunofluorescence analysis corroborated this result and revealed increased cytoplasmic colocalization of Tomm40 with LC3B following the LA treatment. Consistent with these findings, LA significantly suppressed neuroinflammation in LPS-stimulated BV2 microglial cells by inhibiting both NO production and the release of pro-inflammatory cytokines.. Importantly, LA recapitulated its favorable impacts on mitochondrial function and the SIRT3/PINK1/Parkin signaling cascade in this cellular model. The functional necessity of this pathway was demonstrated by the findings that SIRT3 knockdown with siRNA -SIRT3 in BV2 cells abolished regulatory impact of LA on PINK1/Parkin pathway proteins. Conclusions LA serves as a potential therapeutic agent for depression and anxiety through activating mitophagy mediated by the SIRT3/PINK1/Parkin pathway. The results of this study provide scientific evidence for the clinical application of LA in treating depression and anxiety.
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Neural Regeneration Research
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2025
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IF 6.7
Ma Yangguang,Liu Yi,Pan Dongsheng,Zhang Jiawei,Liang Zhuowen,Wang Yi,Hu Xueyu,Wang Zhe,Ding Tan
The blood–spinal cord barrier is crucial for preserving homeostasis of the central nervous system. After spinal cord injury, autophagic flux within endothelial cells is disrupted, compromising the integrity of the blood–spinal cord barrier. This disruption facilitates extensive infiltration of inflammatory cells, resulting in exacerbated neuroinflammatory responses, neuronal death, and impaired neuronal regeneration. Previous research has demonstrated that photobiomodulation promotes the regeneration of damaged nerves following spinal cord injury by inhibiting the recruitment of inflammatory cells to the injured site and restoring neuronal mitochondrial function. However, the precise mechanisms by which photobiomodulation regulates neuroinflammation remain incompletely elucidated. In this study, we established a mouse model of spinal cord injury and assessed the effects of photobiomodulation treatment. Photobiomodulation effectively cleared damaged mitochondria from endothelial cells in mice, promoting recovery of hindlimb motor function. Using microvascular endothelial bEnd.3 cells subjected to oxygen–glucose deprivation, we found that the effects of photobiomodulation were mediated through activation of the PINK1/Parkin pathway. Additionally, photobiomodulation reduced mitochondrial oxidative stress levels and increased the expression of tight junction proteins within the blood–spinal cord barrier. Our findings suggest that photobiomodulation activates mitochondrial autophagy in endothelial cells through the PINK1/Parkin pathway, thereby promoting repair of the blood–spinal cord barrier following spinal cord injury.
研究领域:
神经科学
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再生医学
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细胞生物学
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Chinese Medicine
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2026
·Vol. 21
·期 1
·40
·
IF 5.7
Yao Qianfang,Hu Guishan,Yin Can,Wu Anguo,Hu Guangqiang,Qin Dalian,Zhou Xiaogang,Law Betty Yuen-Kwan,Du Xi,Chen Li,Li Jianqiao,Lin Hong,Long Xin,Wu Jianming,Yu Lu
Background Cerebral ischemia/reperfusion injury (CI/RI) remains a critical barrier to effective ischemic stroke (IS) treatment. While mitophagy activation has been shown to attenuate apoptosis and pyroptosis, thereby ameliorating CI/RI, the therapeutic potential of natural compounds targeting this pathway remains underexplored. Penthorum chinense Pursh (PCP), a traditional hepatoprotective herb, contains Thonningianin A (TA), a bioactive compound with reported autophagic properties. However, the role and mechanisms of TA in CI/RI mitigation remain unclear. Methods In vivo, a middle cerebral artery occlusion/reperfusion (MCAO/R) rat model was established to evaluate TA’s neuroprotective effects via TTC staining, Longa neurological scoring, and immunofluorescence staining. In vitro, oxygen–glucose deprivation/reoxygenation (OGD/R)-treated HT22 and BV2 cells were used to assess TA’s impact on cell viability (MTT, Hoechst/PI staining), mitochondrial oxidative stress (DHE, TMRM, JC-1, Mito-Tracker staining and Western blot), apoptosis (flow cytometry, immunofluorescence staining, Hochest and PI staining and Western blot), and pyroptosis (EthD-2/YO-PRO-1 staining and Western blot). Autophagy and mitophagy modulation was investigated using rapamycin (Rap), 3-MA (autophagy inhibitor), CCCP (mitophagy inducer), and AC220 (mitophagy inhibitor) in EGFP-LC3-U87 and mCherry-GFP-FIS1-293T cells. Co-localization immunofluorescence and Western blotting were employed to validate PINK1/Parkin pathway involvement. Results TA administration significantly improved neurological function, reduced cerebral infarct volume, and attenuated neuronal damage in MCAO/R rats. In vitro, TA suppressed OGD/R-induced mitochondrial oxidative stress and apoptosis in HT22 cells while mitigating pyroptosis in BV2 microglia. Mechanistically, TA activated PINK1/Parkin-dependent mitophagy, as evidenced by enhanced LC3-II/I ratio, and increased mitochondrial-autophagosome co-localization. Crucially, TA’s anti-apoptotic and anti-pyroptotic effects were abolished upon mitophagy inhibition. These findings were corroborated in the MCAO/R model, where TA upregulated PINK1/Parkin signaling and mitigated cell damage. Conclusion This study identifies TA as a novel natural agent alleviating CI/RI by activating PINK1/Parkin-mediated mitophagy, thereby concurrently suppressing apoptosis and pyroptosis. These findings provide the first elucidating the molecular mechanis underlying TA's potential as a therapeutic candidate for IS. Graphical
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Acta Pharmaceutica Sinica B
·
2024
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IF 14.7
Manyu Chen,Yuan Liu,Quanying Liu,Siyan Deng,Yuhan Liu,Jiehao Chen,Yaojia Zhou,Xiaolin Cui,Jie Liang,Xingdong Zhang,Yujiang Fan,Qiguang Wang,Bin Shen
Mitochondrial dysfunction in chondrocytes is a key pathogenic factor in osteoarthritis (OA), but directly modulating mitochondria in vivo remains a significant challenge. This study is the first to verify a correlation between mitochondrial dysfunction and the downregulation of the FOXO3 gene in the cartilage of OA patients, highlighting the potential for regulating mitophagy via FOXO3 gene modulation to alleviate OA. Consequently, we developed a chondrocyte-targeting CRISPR/Cas9-based FOXO3 gene-editing tool (FoxO3) and integrated it within a nanoengineered ‘truck’ (NETT, FoxO3-NETT). This was further encapsulated in injectable hydrogel microspheres (FoxO3-NETT@SMs) to harness the antioxidant properties of sodium alginate and the enhanced lubrication of hybrid exosomes. Collectively, these FoxO3-NETT@SMs successfully activate mitophagy and rebalance mitochondrial function in OA chondrocytes through the Foxo3 gene-modulated PINK1/Parkin pathway. As a result, FoxO3-NETT@SMs stimulate chondrocytes proliferation, migration, and ECM production in vitro , and effectively alleviate OA progression in vivo , demonstrating significant potential for clinical applications.
研究领域:
生物医学工程
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基因治疗
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骨科
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分子生物学
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组织工程
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Acta Pharmaceutica Sinica B
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2023
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IF 14.5
Xiaowei Wang,Mengyan Wang,Meilian Cai,Rongguang Shao,Guimin Xia,Wuli Zhao
Pancreatic cancer is a more aggressive and refractory malignancy. Resistance and toxicity limit drug efficacy. Herein, we report a lower toxic and higher effective miriplatin (MPt)-loaded liposome, LMPt, exhibiting totally different anti-cancer mechanism from previously reported platinum agents. Both in gemcitabine (GEM)-resistant/sensitive (GEM-R/S) pancreatic cancer cells, LMPt exhibits prominent anti-cancer activity, led by faster cellular entry-induced larger accumulation of MPt. The level of caveolin-1 (Cav-1) determines entry rate and switch of entry pathways of LMPt, indicating a novel role of Cav-1 in nanoparticle entry. After endosome-lysosome processing, in unchanged metabolite, MPt is released and targets mitochondria to enhance binding of mitochondria protease LONP1 with POLG and TFAM, to degrade POLG and TFAM. Then, via PINK1-Parkin axis, mitophagy is induced by POLG and TFAM degradation-initiated mitochondrial DNA (mtDNA) replication blocking. Additionally, POLG and TFAM are identified as novel prognostic markers of pancreatic cancer, and mtDNA replication-induced mitophagy blocking mediates their pro-cancer activity. Our findings reveal that the target of this liposomal platinum agent is mitochondria but not DNA (target of most platinum agents), and totally distinct mechanism of MPt and other formulations of MPt. Self-assembly offers LMPt special efficacy and mechanisms. Prominent action and characteristic mechanism make LMPt a promising cancer candidate.
研究领域:
肿瘤学
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药理学
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细胞生物学
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分子生物学
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JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
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2024
·Vol. 28
·期 12
·e18407
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IF 4.3
Zijun Zhou,Qiusheng Zhao,Yuting Huang,Shan Meng,Xin Chen,Guoxin Zhang,Yanbang Chi,Dengyue Xu,Zongtao Yin,Hui Jiang,Liming Yu,Huishan Wang
Chronic intermittent hypoxia (CIH) is associated with an increased risk of cardiovascular diseases. Previously, we have shown that berberine (BBR) is a potential cardioprotective agent. However, its effect and mechanism on CIH-induced cardiomyopathy remain uncovered. This study was designed to determine the effects of BBR against CIH-induced cardiac damage and to explore the molecular mechanisms. Mice were exposed to 5 weeks of CIH with or without the treatment of BBR and adeno-associated virus 9 (AAV9) carrying SIRT6 or SIRT6-specific short hairpin RNA. The effect of BBR was evaluated by echocardiography, histological analysis and western blot analysis. CIH caused the inactivation of myocardial SIRT6 and AMPK-FOXO3a signalling. BBR dose-dependently ameliorated cardiac injury in CIH-induced mice, as evidenced by increased cardiac function and decreased fibrosis. Notably, SIRT6 overexpression mimicked these beneficial effects, whereas infection with recombinant AAV9 carrying SIRT6-specific short hairpin RNA abrogated them. Mechanistically, BBR reduced oxidative stress damage and preserved mitochondrial function via activating SIRT6-AMPK-FOXO3a signalling, enhancing mitochondrial biogenesis as well as PINK1-Parkin-mediated mitophagy. Taken together, these data demonstrate that SIRT6 activation protects against the pathogenesis of CIH-induced cardiac dysfunction. BBR attenuates CIH-induced myocardial injury by improving mitochondrial biogenesis and PINK1-Parkin-dependent mitophagy via the SIRT6-AMPK-FOXO3a signalling pathway.
研究领域:
心脏病学
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药理学
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分子生物学
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MOLECULAR AND CELLULAR BIOCHEMISTRY
·
2024
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IF 3.5
Wang Liwei,Zhang Lu,Yun Yang,Liang Tingting,Yan Chaoqun,Mao Zhuoya,Zhang Jingfang,Liu Baoshe,Zhang Jian,Liang Taigang
Occupational and unintentional exposure of zinc oxide nanoparticles (ZnONPs) raises concerns regarding their neurotoxic potential and there is an urgent need for the development of effective agents to protect against the toxic effects of ZnONPs. Astragalus memeranaceus (AM), a famous Traditional Chinese Medicine, as well as its bioactive components, showing a potential neuroprotective function. This study aims to investigate the neuroprotective effects of bioactive components of AM against ZnONPs-induced toxicity in human neuroblastoma SH-SY5Y cells and its underlying mechanisms. The cell apoptosis, ROS generation, MMP changes, mitochondrial fission/fusion, biogenesis, and mitophagy were assessed. In this study, AM treatment inhibited ZnONPs-induced cell apoptosis and ROS overproduction in SH-SY5Y cells. And astragaloside IV (ASIV) played a dominant role in the attenuation of cytotoxicity after ZnONPs exposure, rather than flavonoids and polysaccharides. ASIV treatment significantly reduced ROS generation and MMP collapse in ZnONPs-exposed cells. Furthermore, the protein expressions of mitochondrial biogenesis (PGC-1α), fusion (Mfn1 and Mfn2), and fission (Drp1) were markedly increased. Meanwhile, the PINK1/Parkin-mediated mitophagy was activated after ASIV administration, which ameliorated ZnONPs-induced SH-SY5Y cell death. Collectively, ASIV administration mitigated ZnONPs-induced cytotoxicity in SH-SY5Y cells through restoring mitochondrial quality control process, which hinted the protective role of ASIV in ZnONPs-induced neurotoxicity. Graphical abstract
研究领域:
药理学
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毒理学
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神经科学
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细胞生物学
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