BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
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2025
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IF 4.2
He Li,Peipei Meng,Yuhang Meng,Yige Yang,Wensheng Zheng,Hongdong Huang,Zhigang Zhao
Renal fibrosis represents a critical pathological hallmark in progressive chronic kidney disease (CKD), yet effective therapeutic strategies remain elusive. Emerging evidence suggests that impaired mitophagy contributes to its pathogenesis. This study investigated whether ruxolitinib alleviates renal fibrosis by enhancing PINK1/Parkin-mediated mitophagy. Network pharmacology was employed to explore the potential regulatory mechanisms of ruxolitinib in renal fibrosis treatment, revealing that ruxolitinib might exert therapeutic effects through modulation of inflammation, oxidative stress and mitophagy. Subsequent in vivo and in vitro studies demonstrated that ruxolitinib treatment not only attenuated renal fibrosis progression but also reduced inflammatory responses and oxidative stress while enhancing mitophagic activity. Mechanistically, the enhancement of mitochondrial autophagy and the amelioration of renal fibrosis by ruxolitinib might be mediated via the PINK1/Parkin pathway. These results suggest that ruxolitinib may ameliorate renal fibrosis by activating PINK1/Parkin-mediated mitophagy, providing new perspectives for CKD therapeutic development.
研究领域:
药理学
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细胞生物学
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肾脏病学
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PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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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.
研究领域:
药理学
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神经科学
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蛋白质组学
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PubMed
高影响因子
Journal of Orthopaedic Surgery and Research
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2025
·Vol. 20
·期 1
·1-17
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IF 2.8
Zhang Yang,Gao Yucheng,Liu Shuanggong,Yang Guowei,Rong Yijun,Wu Dongjin,Gao Zengxin
Background Intervertebral disc degeneration (IVDD) is a multifactorial disorder and a leading contributor to chronic low back pain (LBP), highlighting the need for novel therapeutic strategies. Recent studies indicate that ferroptosis, driven by oxidative stress, plays a key role in the loss of nucleus pulposus cells (NPCs) during IVDD. Vacuole membrane protein 1 (VMP1), a membrane-associated regulator of autophagy, is known to influence various cellular processes. However, its role in IVDD remains unclear. This study investigates the function of VMP1 in IVDD and the mechanisms involved.Methods We established a rat model of IVDD to investigate the correlation between VMP1 expression and ferroptosis during IVDD progression. In vitro, a ferroptosis model of NPCs was induced using tert-butyl hydroperoxide (TBHP) to examine the effects of VMP1 knockdown on NPC apoptosis, extracellular matrix (ECM) degradation, ferroptosis, PINK1/Parkin-dependent mitophagy, and mitochondrial function. Furthermore, cyclosporin A (CsA), a mitophagy inhibitor, was employed to explore the role and potential mechanisms of VMP1 overexpression in regulating PINK1/Parkin-mediated mitophagy, mitochondrial function, and ferroptosis.Results In this study, we observed a significant downregulation of VMP1 expression in a rat model of IVDD, which was accompanied by the occurrence of ferroptosis. Subsequent experiments revealed that VMP1 knockdown aggravated apoptosis and ECM degradation in NPCs. Furthermore, we demonstrated that VMP1 silencing promoted ferroptosis, inhibited PINK1/Parkin-dependent mitophagy, and impaired mitochondrial function in NPCs. In contrast, VMP1 overexpression enhanced PINK1/Parkin-mediated mitophagy, mitigated mitochondrial dysfunction, and suppressed ferroptosis. Notably, these protective effects were abolished by treatment with CsA.Conclusion sThis study demonstrates that VMP1 alleviates IVDD by inhibiting ferroptosis and mitochondrial dysfunction in NPCs, a protective effect mediated through the promotion of PINK1/Parkin-dependent mitophagy. Our study underscores the pivotal role of VMP1 in coordinating mitophagy and ferroptosis during IVDD pathogenesis, identifying VMP1 as a potential therapeutic target for IVDD treatment.Graphical
研究领域:
生物医学
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细胞生物学
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遗传学
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PubMed
高影响因子
Reproductive Sciences
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2025
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IF 2.5
Ma Qianwen,Wu Lifei,Wu Jianfei,Ni Binfei,Wang Jiajia,Song Shiyan
Objective To investigate the mechanism in the progression of decreased ovarian reserve (DOR). Methods Three-month-old female SD rats were employed and randomly divided into the model group and the normal group. The model group was intraperitoneally injected with 4-vinylcyclohexene diepoxide (VCD). Thereafter, blood sample from the abdominal aorta was taken, and rats were sacrificed, and ovarian tissues were obtained by laparotomy. Results HE staining results revealed that the model group exhibited significantly reduced ovarian volume, increased follicular atresia, and decreased quantities of growing follicles and corpus luteum, thereby indicating degraded reserve function of ovarian. TEM images revealed that prominent autophagic vacuoles could be observed in the model group, accompanied by the mitochondria shrinkage and generation of the autophagosome. The expression of Pink1, Parkin, BNIP3L and LC3II genes in ovaries of the model group was significantly higher than those of the normal group ( P < 0.05). In addition, the protein expression of Pink1, Parkin, BNIP3L and LC3II in ovaries of the model group were higher than those of the normal group ( P < 0.05). The expression of Fe 2+ and GSH in oocytes of the model group was higher than those of the normal group ( P < 0.05). The expression of FTH1 and GPX4 in oocytes of the model group was significantly higher than those of the normal group ( P < 0.05). Conclusions Mitochondrial autophagy and ferroptosis may participate in the progression of decreased ovarian reserve (DOR).
研究领域:
生殖生物学
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细胞生物学
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医学
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PubMed
高影响因子
SCIENCE OF THE TOTAL ENVIRONMENT
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2023
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IF 9.8
Xijuan Chao,Dezhi Yao,Chuxuan Chen,Zhiguo Sheng,Benzhan Zhu
Tetrabromobisphenol A (TBBPA), as a widely used brominated flame retardant , has been implicated as a potential neurotoxicant. However, the mechanism of TBBPA-induced neurotoxicity has not been fully elucidated yet. In this study, using mouse hippocampal neuron cell HT22 as the in vitro model, the neuronal cytotoxicity of TBBPA and the mechanism by focusing on mitophagy have been studied. We found that neuronal cytotoxic effects were indeed induced by TBBPA exposure at concentrations of >20 μM for 24 h, including decreased cell viability (to 92.38 % at 20 μM; 18.25 % at 80 μM), enhanced ROS (enhanced 53.26 % at IC 50 of 60 μM, compared with that in the control group) and mitochondrial ROS (mtROS) levels (enhanced 24.12 % at 60 μM), reduced mitochondrial membrane potential (MMP) (decreased 33.60 % at 60 μM). As a protective mechanism in cells, autophagy was initiated; however, mitophagy was inhibited, where PINK1 (PINK1-Parkin activation is critical in the depolarized MMP-induced mitophagy) expression was found to be repressed and decreased, further leading to the failure of Parkin recruitment to the damaged mitochondria. Mitophagy activator, nicotinamide mononucleotide (β-NMN) that activates the PINK1-Parkin pathway, could alleviate TBBPA-induced mitophagy deficiency and further reduce the neuronal cytotoxicity, demonstrating that TBBPA-induced PINK1-Parkin-mediated mitophagy deficiency contributed to the neuronal cytotoxicity. Furthermore, we found TBBPA caused the upregulation of Atf3 ( activating transcription factor 3 ) gene transcription and expression levels, alongside reduced Pink1 levels; whereas enhanced Pink1 transcript levels were observed after ATF3 depletion even under TBBPA treatment, demonstrating TBBPA-induced overexpression of ATF3 should be responsible for the reduced PINK1 expression. Therefore, for the first time, here we demonstrate that TBBPA can inhibit PINK1-Parkin-mediated mitophagy via upregulating ATF3 expression, which further contributes to its neuronal cytotoxicity. This study should be able to improve our understanding of the mechanism of TBBPA-induced neuronal cytotoxicity.
研究领域:
毒理学
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神经科学
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细胞生物学
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PubMed
高影响因子
PHYTOMEDICINE
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2025
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IF 8.3
Qiyue Sun,Ronghua Zhao,Shuran Li,Weiqin Zhou,Jingsheng Zhang,Bo Pang,Shilan Ding,Lei Bao,Zihan Geng,Rui Xie,Dan Xie,Xiaolan Cui,Shanshan Guo,Jing Sun
Background Coronavirus has caused high-mortality viral pneumonia worldwide. The pathogenesis is characterized by hyperinflammatory reactions resulting from immune homeostasis dysregulation. Verbenalin, an iridoid glucoside derived from Verbena officinalis L ., is widely used in Traditional Chinese Medicine (TCM) clinical practice for its antioxidant, anti-inflammatory and antiviral properties. Purpose This study aimed to investigate the pharmacological effects and underlying mechanisms of verbenalin on coronavirus pneumonia both in vivo and in vitro. Methods A coronavirus pneumonia mouse model and macrophage injury models, including mouse alveolar macrophage cell line (MH-S) cells and primary macrophages, were established to initially confirm the antiviral effects of verbenalin. Time-resolved proteomic were then employed to uncover proteomic changes and identify potential therapeutic targets for coronavirus treatment. Subsequently, flow cytometry and Western blot were employed to investigate verbenalin's effects on NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome pathway. Additionally, the targeting regulation of phosphatase and tensin homolog-induced putative kinase 1 (PINK1) / E3 ubiquitin ligase Parkin (Parkin) pathway by verbenalin was validated through molecular docking, surface plasmon resonance (SPR), immunofluorescent staining, RNA interference (RNAi), and mitophagy inhibition both in vivo and in vitro. Results Verbenalin reduced cell injury and inflammation in Human coronavirus 229E (HCoV-229E)-infected macrophages and improved lung inflammation in mice. Proteomics analysis highlighted the roles of nucleotide-binding oligomerization domain (NOD)-like receptor signaling and mitophagy pathways in coronavirus pneumonia. Verbenalin bound strongly to PINK1 and Parkin proteins, increased mitochondrial membrane potential (MMP), decreased mitochondrial reactive oxygen species (mtROS) levels, reduced the opening of mitochondrial permeability transition pore (MPTP), maintained mitochondrial mass, promoted mitophagy flux, upregulated the expression of PINK1, Parkin, and microtubule-associated protein 1A/1B-light chain 3BII (LC3BII). Additionally, verbenalin inhibited the activation of the NLRP3 inflammasome and downregulated the expression of Interleukin-1 beta (IL-1β), cysteine aspartate-specific protease 1 (caspase-1), and gasdermin D (GSDMD) both in vivo and in vitro. Furthermore, treatment with a mitophagy inhibitor and RNAi attenuated the inhibitory effects of verbenalin on NLRP3 activation, confirming the involvement of the PINK1/Parkin/NLRP3 pathway in verbenalin's protective effects. Conclusion Verbenalin enhances PINK1/Parkin-mediated mitophagy to suppress NLRP3 activation, thereby promoting immune homeostasis and mitigating HCoV-229E-induced inflammation.
研究领域:
药理学
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免疫学
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病毒学
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PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2022
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IF 5.195
Zuqing Su,Hongxia Li,Zeting Ye,Ying Zhu,Bing Feng,Lipeng Tang,Guangjuan Zheng
Ethnopharmacological relevance Qidan Tiaozhi capsule (QD), a traditional Chinese medicine , has been used to treat metabolic syndrome for over a decade. However, the mechanism of QD in the treatment of metabolic syndrome is still unknown. Aim of the study Growing studies demonstrate that impaired mitophagy is one of the important causes of metabolic syndrome. Thus, this research aims to investigate the mechanism of mitophagy in the QD treatment of metabolic syndrome. Materials and methods Network pharmacology and molecular docking were used to probe the mechanism of QD treatment of metabolic syndrome. In an oleic acid-induced cell model, glucose consumption and uptake capacity, triglyceride (TG), total cholesterol (TC), malonaldehyde (MDA), superoxide dismutase (SOD) and ROS levels, and mitochondrial membrane potential (MMP) were examined. mRFP-GFP-LC3 adenovirus and GFP-LC3 lentivirus were used to examine the effect of QD on mitophagy. The IRS2-PI3K and AMPK/PINK1-Parkin signal pathways were also determined. What's more, the PINK1 gene was silenced to verify the above findings. In a high-fat diet-fed mouse model, body weight, organ indexes, OGTT, ITT, HOMA-IR, insulin sensitivity, serum MDA, SOD, TC, TG, LDL-C and HDL-C, hepatic TC, TG, LDL-C and HDL-C levels, hepatic steatosis , and IRS2-PI3K and AMPK/PINK1-Parkin signal pathways were investigated. Results Results from network pharmacology and molecular docking suggested that QD might suppress oxidative stress to improve metabolic syndrome. In an oleic acid-induced cell model, compared with the model group, enhanced glucose consumption and uptake ability, inhibited intracellular lipid accumulation, TC, TG, MDA and ROS levels, and increased SOD level and MMP were found in QD groups. And mitophagy levels, IRS2-PI3K and AMPK/PINK1-Parkin signal pathways were promoted. Interestingly, PINK1 silencing reversed the therapeutic action of QD on oleic acid-induced cells. In high-fat diet-fed mice, inhibited body weight, abdominal fat indexes, liver indexes, HOMA-IR, serum and hepatic TC, TG and LDL-C, serum MDA and hepatic steatosis, and increased insulin sensitivity, serum and hepatic HDL-C, serum SOD, and activated IRS2-PI3K and AMPK/PINK1-Parkin signal pathways were found in QD groups. Conclusion QD activates AMPK/PINK1-Parkin-mediated mitophagy to suppress oxidative stress to treat metabolic syndrome.
研究领域:
民族药理学
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代谢生物学
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分子生物学
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PubMed
高影响因子
FOOD AND CHEMICAL TOXICOLOGY
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2025
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IF 3.5
Yue Che,Xiaozhu Wang,Qian Li,Xiyi Peng,Zhen Liu,Wenhui Xu,Mei Jing,Ting Wang,Jian Gao,Weiling Wang
A B S T R A C T Exposure to 4-vinylcyclohexene diepoxide (VCD) has been associated to reproductive toxicity, However, the dynamic ovarian function alterations over time in rats and the underlying mechanisms remain unclear. This study investigated the effects of VCD on ovarian function in female Sprague-Dawley (SD) rats on the 25, 60 and 135 days after VCD injection and discovered related mechanisms. Our results showed that VCD had little ovotoxicity on the 25 th day, as no significant changes were observed except for the reduction of preantral follicles. However, on the 60 th day and 135 th day, rats exhibited irregular estrous cycles, abnormal serum sex hormone levels, ovarian morphological damage, decreased primordial and preantral follicles, and increased atretic follicles. We further found that on the 60 th and 135 th day, VCD might exert ovotoxicity by decreasing antioxidant enzyme levels, inhibiting of the Kelch-like ECH-associated protein 1 (KEAP1)/nuclear factor erythroid 2-related factor 2 (NRF2) and PTEN-induced putative kinase 1 (PINK1)/E3 ubiquitin ligase (Parkin) signaling pathway. Interestingly, on the 25 th day, KEAP1/NRF2 and PINK1/Parking signaling pathway were activated. This study provided a wider application in using laboratory rodents as a model of ovarian failure and highlighted that VCD-induced ovotoxicity was linked to the regulation of the KEAP1/NRF2 and PINK1/Parkin signaling pathways.
研究领域:
生殖毒理学
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分子生物学
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PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
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2025
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IF 4.7
Rihong Luo,Yuhan Kang,He Ma,Zhenqiang Zhang,Christian Hölscher,Li Hao,Zijuan Zhang
To date, no therapeutic drugs available on the market can effectively reverse the progression of Alzheimer's disease (AD). Although Glucagon-like peptide-1 (GLP-1) receptor agonists (RAs) and Cholecystokinin (CCK) RAs have shown some promise in AD research, little is known about the neuroprotective effects of a novel dual CCK/GLP-1 RA in AD. This study sought to examine the effects of the novel dual CCK/GLP-1 RA on cognitive performance in an AD mouse model and to explore the associated mechanisms. Our findings indicate that dual CCK/GLP-1 RA improved cognitive deficits, reduced amyloid-beta (Aβ) accumulation, and alleviated mitochondrial damage in 5 × FAD mice by inducing mitophagy. In an in vitro model of AD cells induced by Aβ, CCK/GLP-1 RA could exert neuroprotective effects by regulating PINK1/Parkin-mediated mitophagy. These data reveal for the first time that the new CCK/GLP-1 RA modulates mitophagy via PINK1/Parkin pathway and enhances cognitive function in the 5 × FAD animal model. Moreover, the performance of the CCK/GLP-1 RA in certain indicators was superior to that of GLP-1 analogue liraglutide, suggesting that it may represent a more promising therapeutic option for AD.
研究领域:
神经科学
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药理学
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分子生物学
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PubMed
高影响因子
JOURNAL OF MOLECULAR HISTOLOGY
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2025
·Vol. 57
·期 1
·11
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IF 2.2
Wang Huan,Han Jian,Li Lin,Li Yan,Yang Jun,Qiu Wangzhong,Yao Liuhua,Zhou Jianjun
Background Shen-Ling-Bai-Zhu-San (SLBZS), a classic formula, shows excellent therapeutic effects on ulcerative colitis (UC). However, its pharmacological mechanism remains unclear. This study aims to explore the SLBZS’s mechanism on mitophagy and inflammation in UC. Method The UC rat model was constructed using 4.5% DSS. The in vivo effects of SLBZS on mitophagy and inflammation were investigated by combining the autophagy inhibitor 3-MA. Caco-2 cells were co-treated with DSS and LPS to mimic UC-like inflammatory. The main active components of SLBZS were analyzed by HPLC. Combined with 3-MA or knockdown of Nrf2, the mechanism by which the main active component of SLBZS Ginsenoside Rg1 affected oxidative stress and inflammation was investigated. Results SLBZS administration alleviated colonic injury in UC rats, reduced disease activity index, increased colonic length, promoted ZO-1, occludin, LGR5, and MUC-2 expressions, decreased ROS production, MDA level, and TNF-α, IL-1β, IL-6, IL-17, and p62 expressions, increased SOD and GSH-PX levels, mitochondrial membrane potential, and PINK1, TOM20, Nrf2, LC3, PINK1, and Parkin levels. 3-MA prevented this phenomenon, indicating that SLBZS inhibited UC inflammation by enhancing mitophagy. The molecular docking results showed that Ginsenoside Rg1 bound to Nrf2. The interaction between Nrf2 and PINK1 was confirmed. Mechanistically, Ginsenoside Rg1 relieved oxidative stress and inflammation in UC-like Caco-2 cell model by Nrf2/PINK1/Parkin pathway-mediated mitophagy. Conclusion Our results indicated that the Ginsenoside Rg1 promoted Nrf2/PINK1/Parkin pathway-mediated mitophagy, thereby alleviating UC, suggesting that Ginsenoside Rg1 could serve as a promising therapeutic agent for clinical UC, with the Nrf2/ PINK1/Parkin axis representing a potential strategy.
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高影响因子
JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE
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2023
·Vol. 103
·期 5
·2367-2377
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IF 4.1
Shun Chen,HuiJuan Liu,JiaQi Zhang,BinBin Zhou,XiaoFang He,Tian Wang,Chao Wang
BACKGROUND This study was conducted to investigate the effect of dietary rutin on the meat quality, antioxidant status and mitochondrial structure and function in the breast muscle of heat-stressed broilers. A total of 192 male broilers were randomly assigned into three groups and treated with normal control (CON), heat stress (34 °C, HS), and HS with 500 mg kg −1 rutin supplementation (HS + Rutin), respectively. RESULTS Dietary rutin significantly reversed HS-induced decrease in body weight, average daily feed intake, average daily gain, and feed efficiency. Rutin supplementation attenuated HS-induced impaired meat quality by decreasing the lightness, drip loss at 24 and 48 h, the peak time of free water ( T 22 ) and the peak area ratio of free water ( P 22 ), and increasing the pH 24h and peak area ratio of immobilized water ( P 21 ). Rutin supplementation promoted superoxide dismutase, glutathione peroxidase activities and total antioxidant capacity, and decreased malondialdehyde levels compared with the HS group. Moreover, rutin attenuated HS-induced mitochondrial damage by increasing the mitochondrial DNA copy number and improving mitochondrial morphology. Dietary rutin significantly increased mitochondrial biogenesis-related mRNA (proliferator-activated γ receptor coactivator-1α [PGC-1α], nuclear respiratory factor 1 [NRF1], and mitochondrial transcription factor A [TFAM]) expression via the AMP-activated protein kinase (AMPK) signaling pathway. HS significantly increased mitophagy-related genes and proteins (Parkin, PTEN-induced putative kinase 1 [PINK1], microtubule associated protein light chain 3-II [LC3-II]) expression, and dietary rutin significantly reversed these alterations. CONCLUSION Dietary rutin attenuated the HS-induced decline in meat quality and antioxidant capacity of broilers, which may be related to inhibition of the AMPK/PINK1–Parkin signaling pathway to attenuate mitochondrial damage. © 2023 Society of Chemical Industry.
研究领域:
动物科学
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营养学
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分子生物学
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PubMed
高影响因子
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
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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.
研究领域:
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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代谢
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PubMed
高影响因子
危险品化学品经营许可证（带存储）