Marine Drugs
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2025
·Vol. 23
·期 3
·134
·
IF 5.4
Yanglong Liu,Jiawei Sun,Qihao Yan,Bingjian Wen,Yan Bai,Qishi Che,Hua Cao,Jiao Guo,Zhengquan Su
Alcoholic liver disease (ALD) is a liver disorder resulting from excessive alcohol intake, and currently, there are no therapeutics approved by the FDA for its treatment. This study investigates the protective effects and underlying pharmacological mechanisms of two chitosan oligosaccharides, COST (MW ≤ 1000 Da) and COSM (MW ≤ 3000 Da), in mitigating alcohol-induced liver disease (ALD). In animal models, we evaluated the changes in ALD following treatment with COST and COSM. Histopathological analysis revealed that both COST and COSM interventions mitigated hepatic steatosis and inflammatory infiltration. Additionally, these compounds reduced various markers of liver injury, enhanced antioxidant enzyme levels, and significantly improved liver function. Western blot analysis demonstrated that COSM markedly decreased the expression of the hepatic metabolic enzyme CYP2E1, activated the Keap-1/Nrf-2/HO-1 pathway, and restrained the NF-κB and MAPK pathways. In an in vitro model of alcohol-induced hepatocyte L02 injury, both COST and COSM exhibited protective effects on hepatocytes, corroborating the findings from the animal studies. Collectively, in vivo and in vitro experiments confirmed that COST and COSM can reduce oxidative damage, enhance antioxidant capacity, and ameliorate steatosis and inflammatory damage in the liver, thereby significantly attenuating alcohol-induced injury. Notably, COSM exhibited slightly superior efficacy compared to COST.
研究领域:
药理学
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肝脏病学
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分子生物学
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高影响因子
Journal of Food Measurement and Characterization
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2024
·
IF 2.9
Meng Wenya,Xue Yuhan,Zhang Jing,Wang Ye,Hou Hu,Li Jing,Dong Ping
Fish sperm extracts have been shown to have various activities, but it has not been effectively developed and utilized at present due to the lack of effective methods for preparing edible grade products. This study proposed a method for preparing edible fish sperm DNA from Alaska pollock (PSD) and evaluated the hepatoprotective effect of the extracted DNA. Firstly, the preparation conditions of fish sperm DNA were optimized by response surface methodology. Under the ideal conditions that the ratio of solid to liquid was 3:1, the pH of extractant was 7.5, the purified solvent was saturated sodium carbonate solution and absolute ethanol was twice the volume of purified solvent, the yield of PSD was (13.657 ± 0.577) µg/mg. To evaluate the liver protective effects of the extracted DNA, the digestion products by three digestion enzymes (pepsin, DNase I and DNase II) compared using an alcohol-induced HepG2 cell model. The DNase I hydrolysis product was more effective in preventing cell alcohol damage, as shown by reducing the content of lipid peroxides. Transcriptomics and metabolomics data revealed that the DNase I hydrolysis product activated the Nrf2/HO-1 pathway through the PI3K/Akt signaling pathway and regulated abnormal lipid synthesis through the steroidogenic pathway. This study will provide an important basis for the evaluation and analysis of the hepatoprotective effect of fish sperm DNA in vivo. Overall, our findings will promote the comprehensive utilization of fish sperm and other aquatic wastes, and provide scientific guidance for the development of functional nucleic acid foods.
研究领域:
食品科学
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分子生物学
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生物化学
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Scientific Reports
·
2024
·Vol. 14
·期 1
·1-15
·
IF 3.8
Wang Yan,Wang Shasha,Ma Chenchen,Qi Weiwei,Lv Jing,Zhang Mengqi,Wang Shibo,Wang Rui,Lu Yangyang,Qiu Wensheng
Gastric cancer (GC) is the most common malignant tumor of the gastrointestinal tract and currently has a poor clinical outcome. Turmeric’s rhizome contains a polyphenolic component called curcumin (Cur), which has been demonstrated to inhibit a variety of tumor cells, such as pancreatic, colon, lung and gastric cancers. However, it remains to be elucidated how Cur functions in GC and what molecular processes underlie it. Here, Cur showed a stronger inhibitory effect on GC cells AGS and HGC27. In addition, Cur’s inhibition of GC cells growth was accompanied by increased ROS production, triggering of the Keap1-Nrf2 signaling pathway, and increased transcription of its downstream antioxidant genes HO-1, GCLM, and NQO1. However, when a ROS scavenger NAC was used, the inhibitory effect of Cur on GC cells was reversed. Nuclear factor erythroid 2-related factor 2 (Nrf2) is overexpressed or activated in cancers to shield cancer cells from oxidative damage by responding to oxidative stress (OS). Cur has been found to act as an activator of Nrf2. Notably, compared with Nrf2 knockdown and Cur alone, the combination of the two dramatically increased Cur-induced ROS overaccumulation and inhibition of GC cells proliferation, migration, and invasive abilities. Consistent with in vitro experiments, Cur combined with Nrf2 knockdown significantly inhibited tumor growth in nude mice transplanted with AGS cells. Therefore, we concluded that Nrf2 depletion enhanced Cur therapy effect in GC by inducing the excessive accumulation of ROS, indicating that this is a promising treatment strategy.
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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癌症治疗
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JOURNAL OF ETHNOPHARMACOLOGY
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2025
·
IF 5.4
Xiaolin Xie,Haikang Fu,Zhixuan Ai,Ziwei Huang,Wenwen Tan,Qingfeng Xie,Yuhong Liu,Yucui Li,Jiannan Chen,Xiaobo Yang,Ziren Su,Zhengquan Lai,Jianhui Xie
Ethnopharmacological relevance Coptidis Rhizome (CR), a cornerstone medicinal herb, is routinely used to treat metabolic diseases for centuries in China. However, the potential mechanism has not been completely elucidated. Preceding investigation has reported that berberine in CR can bind to hemoglobin (Hb) and utilize erythrocyte-Hb self-assembly drug delivery system to significantly upregulate HO-1 expression. Aim of the study This study was designed in a pioneering endeavor to explore the therapeutic potential and underlying mechanism of CR in dexamethasone- and fructose-induced glycolipid metabolism disorders (GLD) rat models. Material and methods The major elements of CR were identified by high performance liquid chromatograph (HPLC). Dexamethasone- and fructose-induced rat GLD model was constructed. Glucolipid metabolism, oxidative status, and insulin sensitivity were investigated. Histopathological, transcriptomic, in silico simulations, immunofluorescence, immunohistochemistry, and Western blotting analyses were performed to gain further mechanism insight. Results HPLC analysis revealed that berberine, palmatine, coptisine, epiberberine, and jatrorrhizine were detected in CR, with berberine as the most abundant. Administration of CR favorably regulated the organ indexes, and significantly improved glucose metabolism by decreasing the FBG and GSP levels along with improved OGTT. CR promoted insulin sensitivity by suppressing the increased levels of FINS, HOMA-IR and ISI, and concomitantly improving ITT. Furthermore, CR normalized lipid metabolism by decreasing the elevated TG, TC and LDL-C levels. Additionally, CR effectively ameliorated histopathological deterioration in pancreatic and hepatic tissues and reduced serum ALT and AST activities. CR also ameliorated oxidative stress by remarkably lowering hepatic ROS fluorescence intensity and serum MDA content, whereas enhancing SOD and CAT enzymatic activity, and T-AOC level. Hepatic transcriptomics analysis revealed the oxidative stress-related gene HMOX1 encoding HO-1 and AMPK pathway critically involved in the therapeutic effect of CR. Furthermore, CR was found to significantly up-regulate the protein expression levels of HO-1, NQO1 and p-AMPK. On the other hand, in silico simulations indicated that strong van der Waals forces interaction between these alkaloids and HO-1. Notably, CR exhibited potent HO-1 agonistic activity comparable to the HO-1 inducer hemin, as manifested by enhanced HMOX1 mRNA level, HO-1 expression level, cytoplasmic HO-1 fluorescence intensity, carbon monoxide production, and reduced heme level, which were the markers of erythrocyte metabolism. Administration of CR or hemin significantly improved fasting glycemia, blood fat, insulin sensitivity, and antioxidant capacity. Nevertheless, these effects were observably reversed by the HO-1 inhibitor zinc protoporphyrin (ZnPP). Conclusion CR effectively ameliorated insulin resistance, hyperglycemia, and dyslipidemia, and its mechanism of action may be at least partially, mediated through HO-1 activation via erythrocyte metabolic regulation. This study provided further evidences for the historical use of CR in the therapy of metabolic diseases. These results highlighted the potential of CR as a novel HO-1 agonist for the development of innovative treatments for GLD.
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REDOX REPORT
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2026
·
IF 6.9
Dongcen Lang,Yanning Zheng,Jing Zhang,Zheng Li,Mengyu Niu,Jian Wang,Xue Wang,Liyong Huang,Jiangyu Xue,Li Li,Ying Chen
Objective Subarachnoid hemorrhage (SAH) is associated with high mortality and poor outcomes, which are closely related to white matter injury (WMI). (-)-Epigallocatechin-3-gallate (EGCG) exerts neuroprotective effects by inhibiting oxidative stress-related ferroptosis in astrocytes and improving neurological function. However, the role and mechanism of EGCG in regulating reactive astrocytes (RAs) to alleviate WMI after SAH remain unclear.Methods A mouse model of SAH was used to evaluate the effects of EGCG-loaded nanoparticles (EGCG-NPs). Western blot, qPCR, and immunofluorescence were performed for biochemical analysis. Neurological function was assessed using neurological deficit scores and the Morris water maze test.Results Following SAH, HO-1-mediated iron accumulation and ROS production promoted A1/A2 reactive astrocyte polarization, resulting in myelination damage and aggravated WMI. Knockdown of S100A10 inhibited iron-dependent oxidative stress in RAs and attenuated WMI. EGCG-NPs significantly suppressed HO-1/S100A10-mediated iron overload and oxidative stress in both A1 and A2 RAs, thereby alleviating WMI after SAH.Conclusion EGCG-NPs attenuate SAH-induced WMI by inhibiting the iron overload-activated HO-1/S100A10 axis in RAs, representing a promising therapeutic strategy.
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Frontiers in Nutrition
·
2026
·
IF 5.5
Maoru Li,Zefeng Wang,Huan Zhai,Jiajiao Li,Ji Ma,Bin Qiu
BackgroundMetabolic dysfunction-associated steatotic liver disease (MASLD) is a rapidly growing metabolic disorder with no FDA-approved treatment. Pachymic acid (PA; synonym: 3-O-acetyltumulosic acid), a lanostane-type triterpenoid, shows potential for treating MASLD. However, its mechanisms remain underexplored.ObjectiveThis work evaluated the therapeutic efficacy and mechanisms of PA in treating MASLD.MethodsThe high-cholesterol diet (HCD)-induced zebrafish model, high-fat diet induced C57BL/6 mice model and free fatty acid (FFA)-treated BRL-3A cells was used to assess PA’s anti- MASLD effects in vivo and in vitro.ResultsPA improved lipid metabolism disrupted by HCD, reduced hepatic oxidative stress, as indicated by decreased MDA levels and increased SOD activity, and lowered inflammatory markers, including TNF-α, IL-6, and IL-1β. PA also enhanced antioxidant activity by regulating the Keap1-Nrf2-HO-1 pathway. PA decreased Keap1 mRNA expression induced by reactive oxygen species (ROS), upregulated Nrf2 and HO-1 expression, and promoted Nrf2 nuclear translocation. These effects suggest that PA inhibits ROS production by activating the Keap1-Nrf2-HO-1 pathway and possibly by inhibiting Nrf2 degradation.ConclusionPA improves MASLD through lipid metabolism regulation and antioxidant effects, primarily by activating the Keap1-Nrf2-HO-1 pathway. These findings highlight PA’s potential as a therapeutic agent for MASLD.
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ARCHIVES OF TOXICOLOGY
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2024
·
IF 4.8
Wang Yanwei,Qiu Jingru,Yan Hua,Zhang Nan,Gao Shixuan,Xu Ning,Wang Cuiyan,Lou Haiyan
Doxorubicin (DOX) is one of the most frequently used chemotherapeutic drugs belonging to the class of anthracyclines. However, the cardiotoxic effects of anthracyclines limit their clinical use. Recent studies have suggested that ferroptosis is the main underlying pathogenetic mechanism of DOX-induced cardiomyopathy (DIC). BTB-and-CNC homology 1 (Bach1) acts as a key role in the regulation of ferroptosis. However, the mechanistic role of Bach1 in DIC remains unclear. Therefore, this study aimed to investigate the underlying mechanistic role of Bach1 in DOX-induced cardiotoxicity using the DIC mice in vivo (DOX at cumulative dose of 20 mg/kg) and the DOX-treated H9c2 cardiomyocytes in vitro (1 μM). Our results show a marked upregulation in the expression of Bach1 in the cardiac tissues of the DOX-treated mice and the DOX-treated cardiomyocytes. However, Bach1 −/− mice exhibited reduced lipid peroxidation and less severe cardiomyopathy after DOX treatment. Bach1 knockdown protected against DOX-induced ferroptosis in both in vivo and in vitro models. Ferrostatin-1 (Fer-1), a potent inhibitor of ferroptosis, significantly alleviated DOX-induced cardiac damage. However, the cardioprotective effects of Bach1 knockdown were reversed by pre-treatment with Zinc Protoporphyrin (ZnPP), a selective inhibitor of heme oxygenase-1(HO-1). Taken together, these findings demonstrated that Bach1 promoted oxidative stress and ferroptosis through suppressing the expression of HO-1. Therefore, Bach1 may present as a promising new therapeutic target for the prevention and early intervention of DOX-induced cardiotoxicity.
研究领域:
药理学
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心脏病学
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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
CELLULAR SIGNALLING
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2025
·
IF 3.7
YaoNan Han,XingTong Wang,DeShui Yu
Spinal cord injury (SCI) is a serious central nervous system disease. Ferroptosis is one of the major causes of spinal cord neurological loss, and targeting ferroptosis is a promising therapeutic strategy. Roflumilast has shown promising applications in the treatment of neurological diseases due to its potent anti-inflammatory and anti-oxidative stress effects. This study aimed to investigate whether roflumilast could inhibit neuronal ferroptosis to improve motor function after SCI in rats. In vitro experiments, we found that roflumilast significantly increased cell survival in an in vitro ferroptosis model, improved mitochondrial function, reduced intracellular iron, reactive oxygen species (ROS), and lipid peroxides accumulation as well as the expression of the pro-ferroptosis proteins, long-chain acyl-coenzyme A synthase 4 (ACSL4), and prostaglandin-endoperoxide synthase 2 (PTGS2), and increased the expression of ferroptosis-inhibitory protein glutathione peroxidase 4 (GPX4), and ferritin heavy chain 1 (FTH1) expression. Mechanistically, these protective effects were achieved by activating AMP-dependent protein kinase (AMPK)/nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling and were attenuated when AMPK signaling was blocked. In vivo experiments, roflumilast attenuated spinal cord tissue damage, increased the number of motor neuron survivors, and improved motor function after SCI in rats. Overall, activation of AMPK/Nrf2/HO-1 signaling by roflumilast attenuated neuronal ferroptosis and improved motor function after SCI in rats.
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高影响因子
NEUROREPORT
·
2020
·Vol. 31
·期 18
·1274-1282
·
IF 1.394
Xi Zhiyu,Chen Xiao,Xu Canxin,Wang Baofeng,Zhong Zhihong,Sun Qingfang,Sun Yuhao,Bian Liuguan
The brain edema following intracerebral hemorrhage (ICH) plays a key role in the recovery process. Protocatechuic acid (PCA) has been proved possessing neuroprotection in ICH. Here we tried to explore its value in brain edema after ICH and reveal underlying mechanisms. ICH model was
created in C57 mice using collagenase IV. PCA was injected intraperitoneally at 30 mg/kg every 24 h in PCA group. On day 3 after ICH, the water content of hemorrhagic ipsilateral hemisphere in PCA group was significantly reduced compared with vehicle group. AQP4, the main water channel, was
remarkably decreased in PCA group. Additionally, ZO-1 and occludin expression were increased in PCA group. The bEnd.3 cells were cultured to understand the effect of PCA on the blood-brain barrier (BBB) integrity. Compare to hemin treated group, plus PCA enhanced the expression of HO-1 and
Nrf2 nuclear translocation. Furtherly, the overexpression of HO-1, ZO-1, occludin, in the PCA treatment group was inhibited after knockdown of Nrf2. Taken together, our results proved PCA alleviated brain edema and BBB disruption in ICH by promoting the Nrf2/HO-1 signaling pathway.
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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高影响因子
NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
·
2023
·
IF 3.6
Zhang Yuying,Zhang Pingping,Zhang Xin,Liu Ye
Honokiol, a bioactive component found in Magnolia officinalis , has shown in protecting against ischemic stroke in animal models. However, its poor water solubility has limited its clinical applications. In this study, we introduced a hydrophilic building block on the aromatic ring of honokiol, resulting in the synthesis of four new compounds (HH-A, -B, -C and -D) with significantly improved water solubility. We then investigated the neuroprotective effects of these compounds in mouse and rat models of transient middle cerebral artery occlusion/reperfusion (tMCAO/R) brain injury. Among the compounds tested, HH-A, also known as (S)-6-((3′,5-diallyl-2,4′-dihydroxy-[1,1′-biphenyl]-3-yl)amino)-6-oxohexane-1,5-diaminium chloride, showed the most promising results. HH-A was found to significantly reduced the infarct volume and brain edema in mice. It also outperformed the other three compounds and honokiol, even surpassing the effects of edaravone dexborneol. Additionally, HH-A demonstrated dose-dependent improvements in body weight, neurological deficits, and infarct volume. Further analysis in tMCAO/R rat model revealed that HH-A treatment led to significant upregulations of Nrf2 and HO-1 in the brain. HH-A also significantly reduced the expression of HNE, and exhibited anti-apoptotic effects by decreasing the expression of Bax and increasing the expression of Bcl-2. This was further supported by a decrease in the number of TUNEL positive cells. Taken together, the neuroprotective effects of HH-A may be attributed to its ability to target the Nrf2/HO-1 signaling pathway, leading to reduced oxidative stress and apoptosis in the brain. These findings suggest that HH-A has potential as a therapeutic agent for the treatment of ischemic stroke.
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PHYTOMEDICINE
·
2022
·
IF 6.656
Xun Sun,Xinyu Zhang,Hui Yan,Hongfei Wu,Shijian Cao,Wenchen Zhao,Ting Dong,An Zhou
Background Hepatolenticular degeneration (HLD) is an autosomal recessive disorder concerning copper metabolism . Copper overload is also accompanied by iron overload in HLD patients , which can lead to ferroptosis . Curcumin , the active component in turmeric, has the potential to inhibit ferroptosis. Purpose The current study proposed a systematic investigation of the protective effects of curcumin against HLD and the underlying mechanisms. Methods The protective effect of curcumin on toxic milk (TX) mice was studied. Liver tissue was observed via hematoxylin-eosin (H&E) staining and the ultrastructure of the liver tissue was observed through transmission electron microscopy . Copper levels in the tissues, serum, and metabolites were measured by atomic absorption spectrometry (AAS). In addition, serum and liver indicators were evaluated. In cellular experiments, the effect of curcumin on the viability of rat normal liver cells (BRL-3A) was determined via the 3-[4,5-dimethylthiazol-2-yl)]-2,5-diphenyltetrazolium bromide (MTT) assay. Cell and mitochondrial morphology were observed in curcumin-mediated HLD model cells. The intracellular copper ion fluorescence intensity was observed via fluorescence microscopy , and intracellular copper iron content was detected using AAS. Further, oxidative stress indicators were evaluated. Cellular reactive oxygen species (ROS) and cellular mitochondrial membrane potential were examined via flow cytometry. Furthermore, the expression levels of nuclear factor erythroid-2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and glutathione peroxidase 4 (GPX4) were determined via western blotting (WB). Results The histopathology of the liver confirmed the hepatoprotective effects of curcumin. Curcumin improved copper metabolism in TX mice. Both serum liver enzyme markers and antioxidant enzyme levels indicated the protective effect of curcumin against HLD-related liver injury. The MTT assay results showed that curcumin was protective against excess copper-induced injury. Curcumin improved the morphology of HLD model cells and their mitochondrial morphology. The Cu 2+ fluorescent probe and the AAS results indicated that curcumin reduced Cu 2+ content in HLD hepatocytes. In addition, curcumin improved oxidative stress levels and prevented the decline of mitochondrial membrane potential in HLD model cells. The ferroptosis inducer Erastin reversed these effects of curcumin. WB revealed that curcumin promoted Nrf2, HO-1, and GPX4 protein expression in HLD model cells, and the Nrf2 inhibitor ML385 reversed the effects of curcumin. Conclusion Curcumin demonstrates a protective role by expelling copper and inhibiting ferroptosis, activating the Nrf2/HO-1/GPX4 signaling pathway in HLD.
研究领域:
药理学
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毒理学
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分子生物学
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细胞生物学
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神经病学
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SOUTH AFRICAN JOURNAL OF BOTANY
·
2026
·
IF 3.1
Xian Dong Lv,Meiherinisa Maitituersun,Fei Li
This study established HPLC fingerprints of PCAE 70% and RLQ, supported by the 2020 edition of the Chinese Pharmacopeia and relevant literature, and performed network pharmacology prediction for the common constituents. • Multi-index regression analysis of uniform design data was conducted by partial least squares, by which seven active components were optimized and determined as six important active components, and their rationality was experimentally validated. • The entropy weight method was employed to unify heterogeneous data from in vitro and in vivo experiments, and the integrated important active component combination was subjected to in vivo activity validation through a mouse urinary tract infection model. • This study suggests that the active components centered on gallic acid, myricitrin, and quercitrin may constitute the major pharmacodynamic material basis of Polygonum capitatum against UTI, and preliminarily explored the underlying mechanism. Ethnopharmacological relevance As a cornerstone herb in the traditional medicine of the Miao ethnic group in Guizhou Province, Polygonum capitatum has long been used to treat diseases of the urinary system. Documented in Miao medical theory as cold in nature and bitter-pungent in taste, and as acting on the kidney and bladder meridians, it is traditionally used to clear heat, promote diuresis, relieve stranguria, and detoxify, thereby relieving pain. The aqueous extract of this herb is the sole component of Relinqing Granules (RLQ), a clinically widespread formulation. Despite its broad clinical application, the underlying material basis of its pharmacological activity remains to be fully elucidated. Materials and methods The target compounds were identified through literature investigation, and their presence in both the Polygonum capitatum 70% aqueous ethanol extract (PCAE 70%) and RLQ was subsequently verified. The common constituents shared by the two were identified by comparing the fingerprint chromatograms with reference standards, and network pharmacology was employed to predict the potential targets of these components. The constituents were then combined through uniform design to evaluate their antibacterial, anti-inflammatory, and antioxidant activities, optimized via partial least squares regression and the entropy weight method, and ultimately validated in a mouse model of UTI. Results A total of seven common constituents were identified: gallic acid, protocatechuic acid, catechin, myricitrin, quercitrin, quercetin, and kaempferol. Network pharmacology predicted that these constituents might exert anti-UTI effects through modulation of the PI3K-Akt signaling pathway. The optimal ratio combination demonstrated significant antibacterial activity against Escherichia coli and Staphylococcus aureus , while another optimal ratio enhanced catalase activity and modulated the expression of AKT-1/Nrf 2 / HO-1/NF-κB 3 in zebrafish. Following data integration using the entropy weight method, mouse validation results revealed decreased TNF-α/IL-1β levels and increased IL-10 levels, with superior efficacy compared to PCAE 70% and RLQ, without dose-dependent differences. The results implied that gallic acid, myricitrin, and quercitrin represent the potential principal active components of P. capitatum. Conclusion The optimized combination dominated by gallic acid, myricitrin, and quercitrin, identified from P. capitatum , exhibited antibacterial, anti-inflammatory, and antioxidant performance superior or equivalent to existing preparations, holding significant theoretical and practical value. Download: Download high-res image (228KB) Download: Download full-size image Graph A illustrates the experimental procedure for determining the in vitro antibacterial activity of target drugs by the MTT method; Graph B illustrates the experimental procedure for the acute toxicity assay in zebrafish; Graph C illustrates the mechanism diagram of drug administration in the zebrafish oxidative stress model; Graph D illustrates the simplified experimental procedure and mechanism diagram before drug administration in the mouse UTI model.
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