CONSTRUCTION AND BUILDING MATERIALS
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2026
·
IF 8.9
Yilin Pi,Yi Li,Wangkun Ma,Cong Lu
To address the early-age strength degradation of low-clinker limestone calcined clay cement (LC3), this study developed a highly reactive and sustainable carbonate source by enhancing the CO 2 mineralization efficiency of carbide slag (CS) through utilizing carboxyl-functionalized carbon nanotubes (CNT-COOH) as growth template. Results showed that the CNT-COOH significantly accelerated the carbonation kinetics of CS. With a 2% dosage of CNT-COOH (by mass of CS), the Ca 2 + concentration in the CS slurry decreased to 410.17 mg/L at 10 min, which was 41.15% lower than that of the reference group. This is because the CNT-COOH induced heterogeneous nucleation of calcite crystals, resulting in a more porous CaCO 3 product layer on the CS surface, thereby providing more channels for the diffusion of CO 2 and Ca 2+ . In low-clinker LC3 systems, the modified CS significantly accelerated hydration kinetics, leading to a 23% and 13.4% increase in the compressive and flexural strength at 1d, respectively. Furthermore, the proportion of harmful pores at 28d was decreased by 20.7%. This is attributed to the promotion of carboaluminate precipitation by the modified CS, as well as the pore refinement resulting from the filling effect of CNT-COOH. This study aims to provide a stable carbonate source for low-clinker LC3, thereby promoting the low-carbon transition of the construction industry.
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高影响因子
ONCOLOGY REPORTS
·
2015
·Vol. 34
·期 6
·3147-3155
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IF 2.301
Lili Zhang,Jie Zhang,Li Chen,Jianli Wang
Autophagy is an intracellular multi-step catabolic degradation process that involves the degradation and recycling of cellular proteins and cytoplasmic damaged organelles to maintain cellular homeostasis and reduction of metabolic stress. Numerous studies have indicated the importance of autophagy in cancer, but the role of autophagy in human skin squamous cell carcinoma (SSCC) development and response to therapy it is still unclear. In the present study, we investigated the role of autophagy in SSCC and the relationship with chemotherapy sensitivity. The present study demonstrated that autophagy related gene the microtubule-associated protein 1 light chain 3 (LC3) expression was low in SSCC. The negative correlation with Bcl2 and survivin, and the chemotherapy drug 5-FU increased the level of autophagy and the autophagy inhibitor 3-MA inhibited this effect in SSCC cells, time- and dose-dependently. When SSCC cells were treated first with 3-MA and then with 5-FU, the inhibition of proliferation, migration, invasion and apoptosis of SSCC cells was enhanced. Our results suggested the possibility of autophagy as a potential target in SSCC therapy and 3-MA and 5-FU combination treatment may be an effective SSCC therapy via autophagy modulating.
研究领域:
肿瘤学
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细胞生物学
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药理学
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PubMed
高影响因子
Genes & Genomics
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2022
·Vol. 44
·期 11
·1375-1384
·
IF 2.164
Wang Yazhuo,Ren Yanan,Li Na,Zhao Jing,Zhao Sufen
Background Rab11a is a novel identified tumorigenic factor involved in different cancers. Objective This study aimed to assess the biological function of Rab11a in ovarian cancer (OC). Methods GEPIA database and real-time PCR were used to determine Rab11a expression in OC tissues and normal ovarian tissues. CCK-8, cell cycle, wound healing, transwell, and enzyme linked immunosorbent assay were used to detect the effects of Rab11a knockdown or overexpression on the proliferation, migration, and invasion of OC cells. Western blot analysis of autophagy-related markers and immunofluorescence staining of LC3 were performed to determine autophagy induction in Rab11a-silenced or overexpressed OC cells. Moreover, autophagy inhibitor 3-MA was employed to clarify the effects of Rab11a-regulated autophagy on the malignant phenotypes of OC cells. Results The mRNA level of Rab11a was increased in tumor tissues from OC patients as compared to the normal ovarian tissues. Knockdown of Rab11a in OVCAR-3 cells inhibited the growth of OC cells and led to cell cycle arrest, accompanied by reduced expression of PCNA and Cyclin D1. Rab11a deficiency suppressed migration and invasion of OC cells, accompanied by decreased secretion of MMP-2 and MMP-9. Silence of Rab11a impeded autophagy induction, as evidenced by decreased LC3 puncta formation, reduced abundance of LC3II and Beclin1, and increased p62 protein expression. In contrast, the ectopic expression of Rab11a in A2780 cells exerted opposite effects. Interestingly, autophagy inhibitor 3-MA abolished the effects of Rab11a overexpression on autophagy, proliferation, migration, and invasion. Conclusions Rab11a promotes the malignant phenotypes of OC cells by inducing autophagy.
研究领域:
肿瘤学
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细胞生物学
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分子生物学
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PubMed
高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2024
·Vol. 25
·期 8
·4493
·
IF 4.9
Jiuge Tang,Dongmei Fang,Jialing Zhong,Min Li
Canonical autophagy is an evolutionarily conserved process that forms double-membrane structures and mediates the degradation of long-lived proteins (LLPs). Noncanonical autophagy (NCA) is an important alternative pathway involving the formation of microtubule-associated protein 1 light chain 3 (LC3)-positive structures that are independent of partial core autophagy proteins. NCA has been defined by the conjugation of ATG8s to single membranes (CASM). During canonical autophagy and NCA/CASM, LC3 undergoes a lipidation modification, and ATG16L1 is a crucial protein in this process. Previous studies have reported that the WDR domain of ATG16L1 is not necessary for canonical autophagy. However, our study found that WDR domain deficiency significantly impaired LLP degradation in basal conditions and slowed down LC3-II accumulation in canonical autophagy. We further demonstrated that the observed effect was due to a reduced interaction between ATG16L1 and FIP200/WIPI2, without affecting lysosome function or fusion. Furthermore, we also found that the WDR domain of ATG16L1 is crucial for chemical-induced NCA/CASM. The results showed that removing the WDR domain or introducing the K490A mutation in ATG16L1 significantly inhibited the NCA/CASM, which interrupted the V-ATPase-ATG16L1 axis. In conclusion, this study highlights the significance of the WDR domain of ATG16L1 for both canonical autophagy and NCA functions, improving our understanding of its role in autophagy.
研究领域:
细胞生物学
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分子生物学
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自噬
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高影响因子
JOURNAL OF INORGANIC BIOCHEMISTRY
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2022
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IF 4.336
Xueru Wang,Ruiming Hu,Chang Wang,Zejing Wei,Shaoxing Pi,Yong Li,Guyue Li,Fan Yang,Caiying Zhang
Excessive molybdenum (Mo) and cadmium (Cd) have toxic effects on animals. However, hepatotoxicity co-induced by Mo and Cd in ducks is still unclear. To evaluate the effects of Cd and Mo co-exposure on autophagy by nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidant defense and endoplasmic reticulum stress (ERS) in duck livers, 40 healthy 7-day-old ducks were randomly assigned to 4 groups and fed diets containing different doses of Mo and/or Cd for 16 weeks, respectively. The results verified that Mo and/or Cd induced oxidative stress via decreasing glutathione peroxidase (GSH-Px), catalase (CAT), and total-superoxide dismutase (T-SOD) activities and increasing hydrogen peroxide (H 2 O 2 ) and malondialdehyde (MDA) concentrations; inhibited Nrf2 axis by downregulating the pathway-related genes and proteins expression levels , and activated ERS through upregulating the protein kinase RNA-like endoplasmic reticulum kinase (PERK)/eukaryotic initiation factor 2a (eIF2a), inositol-requiring enzyme 1 (IRE1) and activating transcription factor 6 (ATF6) pathway-related genes and proteins expression levels, which triggered autophagy via increasing autophagosomes , light chain 3 (LC3) puncta, LC3A, LC3B, autophagy-related gene 5 (Atg5), Bcl-2-interacting protein (Beclin-1) mRNA levels and Beclin-1, microtubule-associated protein light chain 3 II/I (LC3II/LC3I) protein levels, decreasing Dynein, p62 , mammalian target of rapamycin (mTOR) mRNA levels and p62 protein level. Additionally, the changes in Mo and Cd group were the most obvious. Briefly, our study reveals that autophagy induced by Mo and/or Cd may be associated with the activation of crosstalk between Nrf2-mediated antioxidant defense response and ERS in duck livers. Mo and Cd may aggravate toxic damage to the liver.
研究领域:
毒理学
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分子生物学
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兽医学
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PubMed
高影响因子
JOURNAL OF PHARMACY AND PHARMACOLOGY
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2017
·Vol. 69
·期 6
·743-752
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IF 2.405
Wang Meng,Huang Can,Su Yong,Yang Cui,Xia Quan,Xu Du-juan
ObjectivesInhibition of autophagy has been increasingly recognized as a potential therapeutic approach against cancer. Our previous reports showed that Astragaloside II improves hepatic cancer cells resistance by downregulating MDR1 and P-gp .The purpose of this study was to further investigated the effect of autophagy on AS-II reversing multidrug resistance and its molecular mechanism in hepatocellular carcinoma cells in vitro.MethodsBel-7402 and Bel-7402/FU cell lines were used in this study. Western blot was used to detect the expression of autophagy-related protein, p-mTOR and p-p79s6k, MTT was used to analyse cell viability, GFP-LC3 punctate dots distribution was observed by GFP-LC3 transient transfection under fluorescence microscopy and silencing of autophagy-related genes was detected by small interfering RNA transfection.Key findingsAstragaloside II was able to significantly decrease the expression of LC3-II and Beclin-1 in a dose-dependent manner, Astragaloside II (80 μm) further decreased LC3-II formation, Beclin-1 and GFP-LC3 puncta dots stimulated with 5-fluorouracil (0.2 mm) in Bel-7402/FU cells (P < 0.05). In addition, Astragaloside II is capable of sensitizing cells to 5-fluorouracil-induced cell death via inhibition of pro-survival autophagy involvement of MAPK-mTOR pathway.ConclusionsThese findings suggested that Astragaloside II could suppress autophagy by interfering with Beclin-1 and LC3 via MAPK-mTOR pathway, through which sensitized human cancer resistant cells to 5-FU-induced cell death.
研究领域:
肿瘤学
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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
MOLECULES
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2020
·Vol. 25
·期 22
·5302
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IF 3.267
Lili Qin,Tianfeng Lu,Yao Qin,Yiwei He,Ningxin Cui,Ai Du,Jingyu Sun
Resveratrol (RSV) is a natural flavonoid polyphenol compound extracted from the plants which shows various biological activities. However, the clinical application of RSV is limited by its poor aqueous solubility, rapid metabolism and poor bioavailability. In this study, resveratrol-loaded solid lipid nanoparticles (RSV- SLNs) was design as a nano-antioxidant against the physical fatigue. The resultant RSV-SLNs were characterized by photon correlation spectroscopy (PCS), transmission electron micrographs (TEM), zeta potential, differential scanning calorimetry (DSC) and Raman spectroscopy pattern. Furthermore, the in vivo anti-fatigue effect assays showed that RSV-SLNs prolonged the mice exhausted time and running distance. The biochemical parameters of blood related to fatigue suggested that RSV-SLNs have potential applications to improve the antioxidant defense of the mice after extensive exercise and confer anti-fatigue capability. Furthermore, the molecular mechanisms of antioxidant by RSV-SLNs supplementation was investigated through the analysis of silent information regulator 2 homolog 1 (SIRT1) protein expression, which demonstrated that it could downregulate the expression of SIRT1 and increase autophagy markers, microtubule-associated protein 1 light chain 3-II (LC3-II) and sequestosome-1 (SQSTM1/p62). These results reveal that the RSV-SLNs may have great potential used as a novel anti-fatigue sports nutritional supplement.Keywords:solid lipid nanoparticles (SLNs);resveratrol;drug delivery;anti-fatigue;nutrition supplements
研究领域:
药理学
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纳米技术
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运动科学
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营养学
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PubMed
高影响因子
PLoS One
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2018
·Vol. 13
·期 5
·e0197934
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IF 2.766
Xi Chen,Long-Yun Li,Jin-Lan Jiang,Kai Li,Zhen-Bo Su,Fu-Qiang Zhang,Wen-Jing Zhang,Guo-Qing Zhao
In this study, we investigated the relationship between propofol and autophagy and examined whether this relationship depends on ER stress, production of ROS (reactive oxygen species), and disruption of calcium (Ca 2+ ) homeostasis. To this end, we measured C2C12 cell apoptosis in vitro , along with Ca 2+ levels; ROS production; and expression of proteins and genes associated with autophagy, Ca 2+ homeostasis, and ER stress, including LC3 (microtubule-associate protein 1 light chain 3), p62, AMPK (adenosine 5’-monophosphate (AMP)-activated protein kinase), phosphorylated AMPK, mTOR (the mammalian target of rapamycin), phosphorylated mTOR, CHOP (C/BEP homologous protein), and Grp78/Bip (78 kDa glucose-regulated protein). We found that propofol treatment induced autophagy, ER stress, and Ca 2+ release. The ratio of phosphorylated AMPK to AMPK increased, whereas the ratio of phosphorylated mTOR to mTOR decreased. Collectively, the data suggested that propofol induced autophagy in vitro through ER stress, resulting in elevated ROS and Ca 2+ . Additionally, co-administration of an ER stress inhibitor blunted the effect of propofol.
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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高影响因子
BRAZILIAN JOURNAL OF MEDICAL AND BIOLOGICAL RESEARCH
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2024
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IF 1.9
Zheng Delu,Cui Chenli,Ye Chengsong,Shao Chen,Zha Xiujing,Xu Ying,Liu Xu,Wang Can
Coenzyme Q10 (CoQ10) is a potent antioxidant that is implicated in the inhibition of osteoclastogenesis, but the underlying mechanism has not been determined. We explored the underlying molecular mechanisms involved in this process. RAW264.7 cells received receptor activator of NF-κB ligand (RANKL) and CoQ10, after which the differentiation and viability of osteoclasts were assessed. After the cells were treated with CoQ10 and/or H2O2 and RANKL, the levels of reactive oxygen species (ROS) and proteins involved in the PI3K/AKT/mTOR and MAPK pathways and autophagy were tested. Moreover, after the cells were pretreated with or without inhibitors of the two pathways or with the mitophagy agonist, the levels of autophagy-related proteins and osteoclast markers were measured. CoQ10 significantly decreased the number of TRAP-positive cells and the level of ROS but had no significant impact on cell viability. The relative phosphorylation levels of PI3K, AKT, mTOR, ERK, and p38 were significantly reduced, but the levels of FOXO3/LC3/Beclin1 were significantly augmented. Moreover, the levels of FOXO3/LC3/Beclin1 were significantly increased by the inhibitors and mitophagy agonist, while the levels of osteoclast markers showed the opposite results. Our data showed that CoQ10 prevented RANKL-induced osteoclastogenesis by promoting autophagy via inactivation of the PI3K/AKT/mTOR and MAPK pathways in RAW264.7 cells.
研究领域:
细胞生物学
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分子生物学
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药理学
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高影响因子
JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
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2025
·Vol. 39
·期 9
·e70455
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IF 2.8
Lihan Xie,Weinan Li,Shiqi Fan,Jinsong Jin
Diabetic kidney disease (DKD) is a common complication of diabetes, often characterized by podocyte injury, proteinuria, and eventual renal failure. Sinomenine hydrochloride (SH), an active component derived from traditional Chinese medicine, is clinically effective in treating kidney diseases. This study investigates the protective effects of SH on podocytes under high-glucose conditions and its mechanism of action. Mouse podocytes (MPC-5) were treated with SH at concentrations of 50, 200, and 600 μg/mL under high-glucose conditions (30 mmol/L) for 24 h to establish a DKD model. Cell viability was assessed using CCK-8 assays, and apoptosis rates were measured using flow cytometry. Autophagy levels were evaluated by detecting LC3-II, Beclin-1, and P62 proteins via Western blot analysis, while the involvement of the PI3K/AKT/mTOR pathway was analyzed by examining phosphorylated AKT and mTOR. Transmission electron microscopy was employed to observe autophagosomes. SH improved podocyte viability, reduced apoptosis, and enhanced autophagic activity by increasing LC3-II and Beclin-1 expression while decreasing P62 levels. SH also downregulated p-AKT and p-mTOR, indicating inhibition of the PI3K/AKT/mTOR pathway. Electron microscopy confirmed increased autophagosomes in SH-treated groups. SH protects podocytes in a high-glucose environment by enhancing autophagy through inhibition of the PI3K/AKT/mTOR pathway. These findings provide insights into SH as a potential therapeutic agent for DKD management.
研究领域:
药理学
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细胞生物学
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肾病学
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分子生物学
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中医学
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高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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2024
·
IF 5.7
Kun Hu,Shaojun Wu,Jiaxin Xu,Yongzhen Zhang,Yanan Zhang,Xinyuan Wu,Jie Miao,Yongxu Yao,Susu Zhu,Guangtong Chen,Jie Ren
Alzheimer’s disease (AD), one of the neurodegenerative disorders, is highly correlated with the abnormal hyperphosphorylation of Tau and aggregation of β-amyloid (Aβ). Oxidative stress, neuroinflammation, and abnormal autophagy are key drivers of AD and how they contribute to neuropathology remains largely unknown. The flavonoid compound pongamol is reported to possess a variety of pharmacological activities, such as antioxidant, antibacterial, and anti-inflammatory. This study investigated the neuroprotective effect and its mechanisms of pongamol in lipopolysaccharide (LPS)-induced BV2 cells, d-galactose/sodium nitrite/aluminum chloride (d-gal/NaNO2/AlCl3)-induced AD mice, and Caenorhabditis elegans models. Our research revealed that pongamol reduced the release of inflammatory factors IL-1β, TNF-α, COX-2, and iNOS in LPS-induced BV2 cells. Pongamol also protected neurons and significantly restored memory function, inhibited Tau phosphorylation, downregulated Aβ aggregation, and increased oxidoreductase activity in the hippocampus of AD mice. In addition, pongamol reversed the nuclear transfer of NF-κB and increased the levels of Beclin 1 and LC3 II/LC3 I. Most importantly, the anti-inflammatory and promoter autophagy effects of pongamol may be related to the regulation of the Akt/mTOR signaling pathway. In summary, these results showed that pongamol has a potential neuroprotective effect, which greatly enriched the research on the pharmacological activity of pongamol for improving 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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细胞生物学
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PubMed
高影响因子
Molecular Medicine Reports
·
2021
·Vol. 25
·期 2
·1-9
·
IF 2.952
Fa-Xiu Chen,Qin Wan,Qing-Ling Li,Jing Fang,Le Peng,Jian Hu
The function of substance P (SP) in myocardial ischemia is well understood, but its effects on congestive heart failure are unclear. The present study aimed to use in vitro and in vivo approaches to investigate the effects of SP on doxorubicin‑induced cardiomyocyte injury. Pathological changes, apoptosis, cardiomyocyte ultrastructure and molecular mechanisms were evaluated in vitro and in vivo. The effects of SP on cell viability of H9c2 myocardial cells were evaluated using the Cell Counting Kit‑8 and flow cytometry. B‑cell lymphoma 2 (Bcl‑2), Bcl‑2‑associated X protein (Bax), Beclin‑1 and microtubule‑associated protein 1A/1B‑light chain 3 (LC3) were detected by western blotting. Heart failure in rats was established by intraperitoneal injection of doxorubicin. The in vitro data demonstrated that SP at concentrations of 1 µg/ml inhibited doxorubicin‑induced apoptosis of H9c2 cells. Administration of doxorubicin reduced Bcl‑2, Beclin‑1 and LC3 expression levels in H9c2 cells, while having no effect on Bax levels. Administration of SP to these doxorubicin‑treated cells did not affect Bcl‑2 or Bax expression, but further reduced Beclin‑1 while inhibiting the reduction in LC3 expression. In vivo, food intake was significantly increased in rats in the SP group compared with the model group. Cardiomyocytes in the heart‑failure group underwent dysfunctional autophagy as ascertained by transmission electron microscopy. Compared with the heart‑failure group, these pathological changes, including loss of striations and vacuolation, were inhibited by SP treatment, which promoted Bax expression, reduced Beclin‑1 expression and inhibited the reduction in LC3 expression. Taken together, SP reduced cardiomyocyte apoptosis in doxorubicin‑induced cardiomyocyte injury, likely by promoting autophagy, which suggested that SP is a potential therapeutic target for doxorubicin‑induced heart failure.
研究领域:
药理学
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心脏病学
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分子生物学
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细胞生物学
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高影响因子
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