Hepatobiliary & Pancreatic Diseases International
·
2025
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IF 4.4
Han-Ying Zhou,Ting Li,Yuan-Qiang Lu
Background Diquat, a commonly employed bipyridyl herbicide, is recognized for its hepatotoxic effects attributed to the generation of reactive oxygen species. Baicalin (BAI), a flavonoid derivative, has garnered significant research interest for its hepatoprotective properties. Nevertheless, the clinical application of BAI is constrained by its limited water solubility and poor bioavailability. To address these challenges, BAI-nanoliposome (BAI-NL) has emerged as a novel drug delivery platform aimed at enhancing therapeutic outcomes. Methods We used diquat-induced liver injury mouse model and AML12 hepatocytes to test the protective effect of BAI and BAI-NL on liver inflammation, oxidative stress, and mitochondrial function. The parameters included histological, biochemical, and molecular biological analyses. Results In the diquat-induced model, both BAI and BAI-NL exhibited effectiveness on attenuating liver inflammation. Ex vivo analyses further indicated that BAI-NL was superior to BAI in preserving mitochondrial membrane potential, reducing oxidative stress, and modulating the phosphatase and tensin homolog-induced putative kinase 1 (PINK1)/Parkin RBR E3 ubiquitin-protein ligase (Parkin) signaling pathway. These findings enhanced mitophagy and facilitated the removal of damaged mitochondria. Conclusions BAI-NL exhibited superior hepatoprotective effects compared to free BAI, possibly by reducing inflammation, preserving mitochondrial homeostasis, and reinstating autophagic balance through modulation of the PINK1/Parkin signaling pathway. These outcomes indicate a groundbreaking method for addressing liver diseases and underscore the potential of nanoliposome technology in augmenting the efficacy of natural compounds.
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INTERNATIONAL IMMUNOPHARMACOLOGY
·
2025
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IF 4.7
Ziyi Song,Yucheng Gao,Jiangkai Yu,Yang Zhang,Wenbin Xuan,Yijun Rong,Youheng Zhang,Zengxin Gao
This study investigates the role of calreticulin (CRT) in intervertebral disc degeneration (IVDD) and elucidates its underlying mechanisms. CRT expression was markedly reduced in degenerated disc tissues, implicating its involvement in IVDD pathogenesis. Both in vitro and in vivo experiments were conducted to assess the effects of CRT on nucleus pulposus cell (NPC) pyroptosis, apoptosis, and mitochondrial function. Functional analyses demonstrated that CRT overexpression alleviated disc degeneration, inhibited pyroptotic cell death, and preserved mitochondrial integrity. Mechanistically, CRT promoted the clearance of damaged mitochondria through PINK1/Parkin-mediated mitophagy, restoring mitochondrial homeostasis and suppressing ROS accumulation and NLRP3 inflammasome activation. In vivo studies using an IVDD animal model further validated these protective effects, showing reduced disc degeneration and maintenance of extracellular matrix integrity. Recent studies have demonstrated the protective effect of CRT in IVDD. This study builds on these findings and investigates a novel mechanism through which CRT mediates its protective effects in IVDD. Specifically, our study identifies the involvement of PINK1/Parkin-mediated mitophagy in CRT's ability to preserve mitochondrial function and mitigate inflammation in NPCs, offering new insights into the molecular pathways underlying CRT's protective role in IVDD.
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高影响因子
PHYTOMEDICINE
·
2022
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IF 6.656
Zhiguo Mao,Liyu Tian,Jiao Liu,Qian Wu,Ning Wang,Guangyun Wang,Yang Wang,Saiwang Seto
Background Mitophagy plays a critical role in cerebral ischemia/reperfusion by timely removal of dysfunctional mitochondria. In mammals, PINK1/Parkin is the most classic pathway mediating mitophagy. And the activation of PINK1/Parkin mediated mitophagy exerts neuroprotective effects during cerebral ischemia reperfusion injury (CIRI). Ligustilide (LIG) is a natural compound extracted from ligusticum chuanxiong hort and angelica sinensis (Oliv.) diels that exerts neuroprotective activity after cerebral ischemia reperfusion injury (CIRI). However, it still remains unclear whether LIG could attenuates cerebral ischemia reperfusion injury (CIRI) through regulating mitophagy mediated by PINK1/Parkin. Purpose To explore the underlying mechanism of LIG on PINK1/Parkin mediated mitophagy in the hippocampus induced by ischemia reperfusion. Methods This research used the middle cerebral artery occlusion and reperfusion (MCAO/R) animal model and oxygen-glucose deprivation and reperfusion (OGD/R) as in vitro model. Neurological behavior score, 2, 3, 5-triphenyl tetrazolium chloride (TTC) staining and Hematoxylin and Eosin (HE) Staining were used to detect the neuroprotection of LIG in MCAO/R rats. Also, the levels of ROS , mitochondrial membrane potential (MMP) and activities of Na + -K + -ATPase were detected to reflect mitochondrial function. Moreover, transmission electron microscope (TEM) and fluorescence microscope were used to observe mitophagy and the western blot was performed to explore the changes in protein expression in PINK1/Parkin mediated mitophagy. Finally, exact mechanism between neuroprotection of LIG and mitophagy mediated by PINK1/Parkin was explored by cell transfection. Results The results show that LIG improved mitochondrial functions by mitophagy enhancement in vivo and vitro to alleviate CIRI. Whereas, mitophagy enhanced by LIG under CIRI is abolished by PINK1 deficiency and midivi-1, a mitochondrial division inhibitor which has been reported to have the function of mitophagy, which could further aggravate the ischemia-induced brain damage, mitochondrial dysfunction and neuronal injury. Conclusion LIG could ameliorate the neuronal injury against ischemia stroke by promoting mitophagy via PINK1/Parkin. Targeting PINK1/Parkin mediated mitophagy with LIG treatment might be a promising therapeutic strategy for ischemia stroke.
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JOURNAL OF ETHNOPHARMACOLOGY
·
2025
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IF 5.4
Dongchen Xu,Chenyu ShenTu,Chuhong Zong,Weiliang Fu,Jiawei Ling,Ping Shao,Xuesong Liu,Yong Chen,Tengfei Xu
Ethnopharmacological relevance Salvia miltiorrhiza Bunge, a traditional Chinese medicine, has been utilized in the treatment of Parkinson's disease (PD) for thousands of years, as evidenced by its inclusion in ancient formulas such as YangXue XingNao Tang and XingGan ZhenFeng Tang . However, the underlying mechanisms of its therapeutic effects on PD remain unclear. Aim of the study This study aims to evaluate the therapeutic effects of Salvia miltiorrhiza Bunge on a rotenone-induced PD rat model and elucidate its mechanism of action. Methods To explore the efficacy of Salvia miltiorrhiza Bunge extract (SME) in PD, we employed both in vitro and in vivo models using rotenone-induced PC12 cells and rats. Therapeutic effects were assessed through cell viability assays, behavioral tests, and immunohistochemistry. Proteomic analysis and molecular docking experiments were conducted to identify the pathways involved in SME's effects. Immunofluorescence and Western blotting were used to validate the role of mitophagy, while transmission electron microscopy (TEM) provided direct evidence of mitophagy induction by SME. Results Salvia miltiorrhiza Bunge significantly improved motor dysfunction and mitigated dopaminergic neuron degeneration in the substantia nigra of rotenone-exposed rats. Proteomic analysis revealed significant activation of the PINK1/Parkin pathway following SME treatment. Furthermore, molecular experiments confirmed that SME induces mitophagy, which protects PC12 cells from rotenone-induced damage. Conclusion This study demonstrates the therapeutic efficacy of Salvia miltiorrhiza Bunge in mitigating PD-related pathologies. Through proteomic and molecular analyses, we identified SME's ability to activate the PINK1/Parkin pathway and promote mitophagy, offering new insights into its mechanism of action in PD.
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ENVIRONMENT INTERNATIONAL
·
2026
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IF 9.7
Helei Cai,Shihao Luo,Zhengrong Zhou,Feixia Chen,Jiawei Ying,Qiufang Wu,Yize Wu,Shihua Chen,Xinxin Yao,Feiqin Xie,Wenhui Xu,Ke Xu,Renyi Peng
Perfluorooctanoic acid (PFOA) and perfluorobutyric acid (PFBA), as representative long-chain and short-chain per- and polyfluoroalkyl substances (PFAS), are widely distributed in the environment. These compounds can interact with nanoplastics (NPs) to form complex mixed pollutants, posing potential threats to aquatic organisms and human health. The nervous system, characterized by high sensitivity and energy dependence, is particularly vulnerable to such pollutants. However, the mechanisms underlying neurological toxicity induced by co-exposure to PFOA, PFBA, and NPs remain largely unclear. In this study, zebrafish larvae and human neuroblastoma SH-SY5Y cells were employed as model systems to systematically evaluate the effects of PFOA and PFBA, alone or in combination with NPs, on neural development, behavior, cell viability, mitochondrial function, and autophagy. The results demonstrated that NPs exhibited a significantly higher adsorption capacity for PFOA than for PFBA, and that co-exposure exacerbated neurodevelopmental impairments, behavioral abnormalities, and reductions in cell viability. At the molecular level, co-exposure markedly inhibited the PINK1/Parkin-mediated mitophagy pathway, resulting in mitochondrial damage accumulation, disruption of energy metabolism, and blockade of autophagic flux. Through PINK1 overexpression and pharmacological activation experiments, the pivotal role of the PINK1/Parkin-mediated mitophagy pathway in mitigating neurotoxicity was functionally validated. Collectively, this study elucidates the molecular mechanism by which co-exposure to PFOA, PFBA, and NPs induces neurotoxicity via suppression of mitophagy. These findings identify a potential molecular target for the prevention and treatment of PFAS- and NPs-induced neurological injury and provide valuable theoretical and experimental evidence for evaluating the neurotoxic risks of mixed environmental pollutants.
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JOURNAL OF ETHNOPHARMACOLOGY
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2026
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IF 6.8
Deng Yu,Tao Yongjian,Qing Yali,Wang Jianwei,Jie Chuanhong
Ethnopharmacological relevance Diabetic retinopathy (DR) is a severe microvascular complication of diabetes that is closely associated with hyperglycemia-induced mitochondrial dysfunction. Lishui Xiaozhong granules (LSXZ) are an empirical traditional Chinese medicine used to treat DR. However, its precise molecular targets and underlying mechanisms remain unclear. Aim of the study This study investigated whether LSXZ protects retinal cells under hyperglycemic conditions by regulating PINK1/Parkin-mediated mitophagy. Materials and methods Human Müller cells were exposed to high glucose (HG; 50 mM) to establish an in vitro model and treated with LSXZ-containing serum and the mitophagy inhibitor cyclosporin A (CsA). Genetic knockdown via siRNA was performed to validate the necessity of the PINK1/Parkin pathway. A zebrafish DR model was induced using an HG, high-fat diet, and treated with different LSXZ concentrations. Cell viability, mitophagy, apoptosis, ferroptosis, mitochondrial function, and ultrastructural changes were assessed using CCK-8 assays, western blotting, qPCR, immunofluorescence, and transmission electron microscopy. Retinal histopathology, vascular diameter, inflammatory cell activation, oxidative stress, and gene expression profiles in zebrafish were assessed using hematoxylin–eosin staining, fluorescence microscopy, and transcriptomic sequencing. Results LSXZ treatment reversed pathological changes by restoring PINK1/Parkin signaling, elevating LC3-II/LC3-I ratio, enhancing mitochondrial function, and suppressing apoptosis and ferroptosis—effects partially attenuated by CsA. Mitophagosomes increased after LSXZ treatment. Crucially, specific knockdown of PINK1 or Parkin significantly abolished LSXZ-induced cytoprotection, reversing the regulation of apoptotic/ferroptotic markers and mitochondrial recovery, thereby confirming the pivotal necessity of this pathway. In zebrafish, LSXZ alleviated hyperglycemia-induced retinal inner nuclear layer thinning, vascular dilation, excessive macrophage/astrocyte activation, and oxidative stress. These protective effects were mediated through upregulation of the TOMM40/TOMM20–PINK1/Parkin–MFN2 axis.
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高影响因子
MOLECULAR NEUROBIOLOGY
·
2026
·Vol. 63
·期 1
·454
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IF 5.5
Yu Jia-Xin,Zhang Wen-Xuan,Li Pu-Yu,Yang Yi-Liang,Huang Han-Chang
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized primarily by deterioration in memory, cognition, and learning ability. Its etiology is complex and influenced by multiple factors, including genetics and environment. With advancing research into mitochondrial function and mechanisms, impaired mitophagy has been proposed as a significant mechanism contributing to AD. The ApoE ε4 allele, a high-risk genetic factor for AD, may play a key role in disease pathogenesis by inducing mitophagy dysfunction and apoptosis. From the perspective of APOE gene polymorphisms, this study investigates abnormal changes in mitochondrial function and autophagy in humanized APOE4 mice primary astrocytes under oxidative stress, as well as the regulatory effect of curcumin (Cur) on mitophagy and oxidative stress-induced apoptosis, thereby exploring its potential to ameliorate AD through targeting mitophagy. Mitochondrial function analysis revealed that APOE4 expression reduced the antioxidant capacity and respiratory function of primary astrocytes, leading to mitochondrial membrane damage, intracellular reactive oxygen species (ROS) accumulation, and decreased ATP production. Curcumin effectively protected mitochondrial integrity, reduced the number of damaged mitochondria, improved overall mitochondrial function, and helped maintain mitochondrial homeostasis involving in PINK1/Parkin pathway. Regarding autophagy and apoptosis, curcumin was shown to restore autophagic flux, mitigate autophagy disruption caused by oxidative stress, and reverse early-stage apoptosis. Graphical
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MOLECULAR NEUROBIOLOGY
·
2026
·Vol. 63
·期 1
·432
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IF 5.5
Lin Jinyu,You Bowen,Yang Xin,Li Xue,Sun Wenjuan,Xu Zhongyu,Zhang Yi,Tong Xuhui,Dong Shuying
Cerebral ischemia/reperfusion injury (CIRI) refers to the secondary brain injury that occurs when blood supply is restored to ischemic cerebral tissue, and represents one of the primary causes of adult disability and mortality. Current evidence indicates that aesculin exhibits antioxidative and anti-inflammatory activities; however, its therapeutic effects on CIRI remain to be elucidated. The objective of this study was to investigate the potential role of Esculin (ESCU) in protecting against CIRI and to elucidate its underlying mechanisms. Adult male mice were used to establish the middle cerebral artery occlusion/reperfusion (MCAO/R) model. The mice were administered varying doses of ESCU or a reference positive control drug. To evaluate the neuroprotective effects of ESCU, neurological deficit scores were assessed, and cerebral blood flow was measured. 2,3,5-triphenyltetrazolium chloride staining, H&E staining, and Nissl staining were used to determine neuronal damage. NLRP3-related markers and mitophagy-related markers were determined to investigate the mechanism of action of ESCU. ESCU afforded robust neuroprotection in mice, ameliorating functional deficits, reducing infarct size, and preserving neuronal structure. It potently alleviated oxidative stress and restored mitochondrial function (reduced ROS, improved cristae morphology, and increased mitochondrial membrane potential). Mechanistically, ESCU activated mitophagy (upregulating LC3Ⅱ, PINK1, and Parkin; downregulating p62) and inhibited the NLRP3 inflammasome (downregulating NLRP3, GSDMD-N, cleaved caspase-1, IL-1β, and IL-18). Notably, the mitophagy inhibitor Mdivi-1 abolished ESCU’s inhibition of the NLRP3 pathway, establishing a causal relationship. Thus, ESCU mitigates cerebral ischemia-reperfusion injury by coordinately enhancing mitophagy and suppressing NLRP3 inflammasome activation. Our study demonstrates that ESCU attenuates CIRI mechanistically by promoting PINK1/Parkin-mediated mitophagy, thereby suppressing NLRP3 inflammasome activation. These findings not only elucidate a novel pathway underlying ESCU’s neuroprotection but also position it as a promising therapeutic candidate for CIRI, warranting further investigation into its precise targets and clinical potential.
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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
·
2024
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IF 2.5
Mengyun Dong,Tianliang Zhang,Xueli Liang,Xinyi Cheng,Fuyan Shi,Hang Yuan,Fengxiang Zhang,Qiqi Jiang,Xia Wang
Sesamin, a special compound present in sesame and sesame oil, has been reported a role in regulating lipid metabolism, while the underlying mechanisms remain unclear. Autophagy has been reported associated with lipid metabolism and regarded as a key modulator in liver steatosis. The present work aimed to investigate whether sesamin could exert its protective effects against lipid accumulation via modulating autophagy in HepG2 cells stimulated with oleic acid (OA). Cell viability was evaluated using the CCK-8 method, and triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein, cholesterol (LDL-C), alanine aminotransferase (ALT), along with aspartate aminotransferase (AST) were assessed by oil red O staining, transmission electron microscopy (TEM), and biochemical kits to investigate the lipid-lowering effects of sesamin. Differentially expressed genes were screened by RNA sequencing and validated using real-time quantitative PCR and Western blot. Autophagy and mitophagy related molecules were analyzed employing TEM, Western blot, and immunofluorescence. The data shows that in HepG2 cells stimulated by OA, sesamin reduces levels of TG, TC, LDL-C, ALT, and AST while elevating HDL-C, alleviates the lipid accumulation and improves fatty acid metabolism through modulating the levels of fat metabolism related genes including PCSK9, FABP1, CD36, and SOX4. Sesamin restores the suppressed autophagy in HepG2 cells caused by OA, which could be blocked by autophagy inhibitors. This indicates that sesamin improves fatty acid metabolism by enhancing autophagy levels, thereby mitigating the intracellular lipid accumulation. Furthermore, sesamin significantly enhances the mitophagy and improves mitochondrial homeostasis via activating the PINK/Parkin pathway. These data suggest that sesamin alleviates the excessive lipid accumulation in HepG2 caused by OA by restoring the impaired mitophagy via the PINK1/Parkin pathway, probably playing a preventive or therapeutic role in hepatic steatosis.
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高影响因子
PHYTOMEDICINE
·
2025
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IF 8.3
Lu Bocheng,Chen Yongfu,Cai Junjie,Li Ziqi,Guo Lina,Qu Tingli,Tang Li,Zheng Qian
Objective Guzhi Zengsheng Zhitong Decoction (GZZD) is a classic traditional Chinese medicine (TCM) prescription for treating knee osteoarthritis (OA), and has been widely used in clinical practice in China. Given that Forkhead box protein O 1 (FoxO1) has been identified as a potential therapeutic target for OA treatment, this study investigates the chondroprotective effects of GZZD through FoxO1-mediated mitochondrial regulation, bridging traditional medicine with contemporary molecular insights. Methods The therapeutic effects of GZZD on OA and its chondroprotective mechanisms were evaluated both in vivo and in vitro . A rat model of knee OA was established by intra-articular injection of monosodium iodoacetate (MIA), while an in vitro OA model was induced by IL-1β stimulation in chondrocytes. Histological staining, immunohistochemistry, and Western blot analyses were performed to assess cartilage protection. Serum ingredients of GZZD were identified using LC-MS/MS, and the core pathways involved in GZZD-mediated chondroprotection were explored through transcriptomics and network pharmacology. Key protein expression was examined, and molecular biology techniques were applied to validate the role of FoxO1 and its downstream pathways in regulating chondrocyte autophagy, apoptosis, and mitochondrial dysfunction. Additionally, molecular docking and molecular dynamics simulations were conducted to analyze interactions between bioactive compounds and FoxO1. Results GZZD significantly ameliorated MIA-induced knee joint damage, reduced cartilage degradation and subchondral bone destruction, and decreased OARSI scores. Treatment with GZZD markedly decreased serum levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) while enhancing protective autophagy in chondrocytes. Furthermore, GZZD inhibited chondrocyte apoptosis and mitochondrial dysfunction, accompanied by the upregulation of the cartilage matrix protein COL2A1 and the anti-apoptotic protein BCL2, along with downregulation of catabolic factors (MMP13, IL-1β). Mechanistically, GZZD activated the FoxO1/PINK1/Parkin pathway, restoring mitochondrial homeostasis and mitigating mitochondrial-dependent apoptosis, ultimately protecting chondrocytes from OA-related damage. Conclusion For the first time, this study demonstrates that the traditional Chinese medicine formula GZZD alleviates osteoarthritis by activating the FoxO1/PINK1/Parkin pathway, thereby restoring mitochondrial function and protecting chondrocytes from injury. These findings not only establish GZZD as a promising complementary therapy for OA but also provide a scientific foundation for developing FoxO1-targeted therapeutics.
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高影响因子
Foods
·
2025
·Vol. 14
·期 24
·4173
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IF 5.1
Cuicui Zhuang,Jinhui Zhao,Xinying Zhang,Mingyue Guo,Yiguang Lu,Ting Pei,Yangfei Zhao,Chen Liang,Jianhai Zhang
Long-term excessive fluoride intake from food causes skeletal fluorosis, which manifests as bone sclerosis, deformation, joint dysfunction, and even disability. Mitophagy and ion homeostasis regulate bone function. This study investigated the role of melatonin (MLT) in mitigating this condition, given its known involvement in bone remodeling and the fact that fluoride impairs its synthesis in the pineal gland. Firstly, network pharmacology and molecular docking identified mitophagy as MLT’s key pathway against sodium fluoride (NaF)-induced osteosclerosis. Subsequently, a 400 mg/kg/day body weight NaF exposure model in chicken model with 25 mg/kg/day body weight MLT intervention were established in the current study. Fluoride exposure caused the disturbance of ion homeostasis, and the impairment of mitochondria and activation of PTEN-induced putative kinase1 (PINK1)/E3 ubiquitin ligase Park2 (Parkin)-mediated mitophagy in the bone. Importantly, these deleterious effects were significantly restored by MLT supplementation. In conclusion, NaF causes bone injury via ion homeostasis disruption, osteoblast mitochondrial damage, leading to excessive mitophagy. MLT inhibits fluoride-induced mitophagy through the calcium ion flow-mediated PINK1/Parkin pathway, mitigating bone damage. This study can not only ensure the safety of animal-derived food but also provide a theoretical basis for the prevention and treatment of fluorosis in humans and animals.
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JOURNAL OF SLEEP RESEARCH
·
2024
·
IF 3.4
Honglin Jia,Xu Chen,Zhengting Liang,Ruining Liang,Jinhong Wu,Yanling Hu,Wenjun Cui,Xingping Zhang
Summary GAD67 impacts insomnia as a key enzyme catalysing the conversion of glutamate (Glu) to gamma-aminobutyric acid (GABA). Senegenin enhances neuroprotection and is used widely to treat insomnia and other neurological diseases. This study aimed to investigate how senegenin regulates insomnia through a GAD67-mediated signalling pathway. We measured GAD67 expression levels in insomnia patients and evaluated the expression levels of GAD67 and Keap1/Nrf2/Parkin/PINK1-related cytokines following GAD67 lentiviral transfection in PC12 cells and in rat models. We also assessed cellular reactive oxygen species (ROS) and mitochondrial membrane potential levels. Additionally, EEG/EMG was used to analyse the sleep phases of rats and to assess memory and exploration functions. Pathological changes and the expression of GAD67 and sleep-related proteins in the hippocampus were examined. The results showed that GAD67 expression was increased in insomnia patients, ROS levels were elevated, and the mitochondrial membrane potential was decreased in the GAD67-KD group. Insomnia rats exhibited changes in sleep rhythm, learning, and exploration dysfunction, pathological changes in the CA1 region of the hippocampus, and differential expression of GAD67 and sleep-related factors. Inhibitory neurofactor expression levels were decreased in insomnia rats, showing a positive correlation in the GAD67-KD group and a negative correlation in the GAD67-OE group. Conversely, excitatory factor expression levels were increased in insomnia rats, showing a positive correlation in the GAD67-KD group and a negative correlation in the GAD67-OE group. Senegenin intervention modulated cytokine expression levels. In conclusion, GAD67 negatively regulates insomnia, and senegenin can regulate insomnia by mediating the expression of cytokines in the GAD67-regulated Keap1/Nrf2/Parkin/PINK1 pathway.
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