Communications Biology
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2026
·Vol. 9
·期 1
·390
·
IF 5.8
Li Keying,Zhao Xinying,Xie Zhuoyi,Wu Qiuchen,Jia Wenlu,Zhou Xiangrong,Gao Xiang,Zeng Ping,Li Jing,Niu Qiao,Qi Zhipeng,Cui Mengqiao,Song Weiyi
Lanthanum (La), the second most produced rare earth element, is detected in various environmental and human samples. Epidemiological studies have reported a strong association between La exposure and liver injury. However, the effects of early La exposure on liver development and underlying mechanisms remain limited. Here, we evaluate the hepatotoxicity of LaCl 3 at environmentally relevant concentrations using zebrafish larvae. Embryonic LaCl 3 exposure causes concentration-dependent hepatic steatosis, which cannot be reversed after exposure cessation. Metabolomic profiling reveals that very-low-density lipoprotein (VLDL) and its multiple downstream metabolites are consistently downregulated upon LaCl 3 treatment, together with increased triglycerides (TG) level, indicating impaired TG-VLDL biosynthesis. In addition, transcriptomics suggest that genes related to the PPAR α signaling pathway are significantly downregulated, especially those involved in TG-VLDL biosynthesis ( mttp and all apob subtypes). Further studies show that LaCl 3 can inhibit the transcriptional regulatory activity of PPAR α . The upregulation of the PPAR α signaling pathway corresponding genes of ppara , mttp , and apob effectively rescues LaCl 3 -induced liver impairments. Subsequently, a subcellular localization assay finds that increased ApoB degradation in the endoplasmic reticulum contributes to LaCl 3 -triggered lipid droplet accumulation. Overall, our findings fill critical research gaps regarding LaCl 3 -induced hepatotoxicity and provide important evidence for the environmental risk assessment of La.
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Frontiers in Pharmacology
·
2026
·
IF 5.4
Binwei Jin,Yang Zhang,Jiangbo Lin,Yu Zhu,Mengqi Yang,Yutao Zhang,Yanping Yin,Zhiming Zhang,Minjun Yang,Jianjun Jiang,Yafei Mi
Background Myocardial ischemia-reperfusion injury (MIRI) remains a therapeutic challenge with limited treatment options. Ferroptosis, characterized by lipid peroxidation, contributes significantly to MIRI pathogenesis. This study investigates whether dihydromyricetin (DHM), a bioactive flavonoid from Ampelopsis grossedentata , alleviates MIRI by inhibiting ferroptosis, and explores its cardioprotective mechanisms. Methods A mouse myocardial I/R model was established in vivo by ligating the left anterior descending coronary artery for 30 min, followed by reperfusion for one or 7 days. Mice were pretreated with DHM (125 or 250 mg/kg, gavage) for 4 weeks, or with Fer-1 (10 mg/kg) for 1 week. In vitro , an OGD/R model was constructed using H9c2 cells, which were then treated with DHM (0–200 μM) or Fer-1 (10 μM). Potential targets were screened via network pharmacology. Target interaction was validated through biotin-pull-down, molecular docking, CETSA, and DARTS assays. Functional validation was performed using PPARα-knockdown and rescue cell lines. Results GSEA indicated significant activation of the ferroptosis pathway in MIRI, and cellular experiments confirmed that OGD/R induced a typical ferroptosis phenotype. DHM dose-dependently reversed OGD/R-induced ferroptosis-related alterations and ameliorated mitochondrial ultrastructural damage. In vivo , DHM pretreatment significantly reduced serum CK-MB levels, myocardial infarct size, and histopathological injury in I/R mice, while reversing cardiac ferroptosis marker changes. Mechanistically, network pharmacology identified seven overlapping targets, among which DHM specifically reversed the downregulation of PPARα. Biochemical assays and molecular docking confirmed that DHM directly binds to and stabilizes PPARα via the E286 site. Knockdown of PPARα markedly attenuated the anti-ferroptotic and cardioprotective effects of DHM, whereas PPARα rescue partially restored its function. Conclusion This study demonstrates for the first time that DHM alleviates ischemia-reperfusion injury by directly targeting the E286 site of PPARα, upregulating its levels, and thereby suppressing cardiomyocyte ferroptosis. This finding reveals a novel mechanism underlying the cardioprotective effect of DHM and provides a new theoretical basis for targeting the PPARα-ferroptosis axis in MIRI intervention.
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Journal of Functional Foods
·
2025
·
IF 4
Hanju Fan,Meng Yan,Yongshuai Jing,Ziyan Li,Yaqian He,Zhiwei Li,Junna Song,Lanfang Wu
Crataegus pinnatifida is the dried fruit of Crataegus pinnatifida . Crataegus pinnatifida polysaccharides (CPPs) eluted with water as the mobile phase (CPPs-H-1) is one of the important active components. CPPs-H-1 has anti-oxidation and blood lipid regulation activities in vitro. Therefore, we investigated the effects of CPPs-H-1 on nonalcoholic fatty liver disease (NAFLD) in C57/BL6J mice. As a result, CPPs-H-1 inhibited the rapid growth of body weight and alleviated the liver injury caused by high-fat diets, significantly reducing the liver index and blood lipid levels in the model group, inhibiting the production of inflammation and cytokines, and inhibiting oxidative stress. CPPs-H-1 also enhanced intestinal barrier function. At the phylum level, CPPs-H-1 reduced the ratio of Firmicutes to Bacteroides (F/B) and regulated the content of short-chain fatty acids (SCFAs). The CPPs-H-1 may regulate intestinal flora composition, and improve intestinal barrier function, ultimately delaying the progression of NAFLD in mice. Also, CPPs-H-1 improved NAFLD progression by enhancing the Amp-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor α (PPARα) signaling pathway to enhance fatty acid oxidation. All these results confirm that CPPs-H-1 plays a multi-pathway and multi-target role in the improvement of NAFLD.
研究领域:
营养学
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分子生物学
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药理学
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BIOCHEMICAL PHARMACOLOGY
·
2026
·
IF 6.5
HaoranZhong,Lei Sun,Jiajun Yu,Yanrong Wang,Tongjie Xu,Tingfeng Yang,Niangkun Liu,Jiayuan Chen,Jinwu Liu,Haochen,Wenguang Fu
Liver regeneration is essential for recovery after major resection or acute injury, yet early regenerative failure remains common. Ferroptosis, an iron-dependent form of lipid peroxidation-driven cell death, impairs hepatocyte survival and may constrain regeneration. Naringenin (NAR), a citrus flavonoid with hepatoprotective activity, has been reported to modulate oxidative stress; however, whether it supports liver regeneration through ferroptosis modulation and which upstream targets are involved remains unclear. Here, hepatocyte models (AML12, Huh7, HepG2) and a murine 70% partial hepatectomy (PHx) model were used to investigate the involvement of PPARα signaling. Proliferation was assessed by CCK-8, EdU, and cell-cycle proteins. Ferroptosis-associated readouts (Fe 2+ , MDA, ROS, GSH) were measured following RSL3 exposure with or without NAR, ferrostatin-1, fenofibrate, or GW6471. Target identification involved network pharmacology, molecular docking, protease protection assay, and CETSA. In PHx mice, NAR was associated with improved liver regrowth (LW/BW ↑25% at 48 h), reduced ALT/AST (∼30–40%), increased proliferation markers, elevated GSH/CAT, and decreased Fe 2+ /MDA. In vitro, NAR increased GPX4/SLC7A11 expression and attenuated RSL3-induced ferroptosis-associated changes. These effects were mimicked by fenofibrate and attenuated by GW6471. NAR was associated with increased PPARα stability and expression. These findings suggest that NAR is associated with reduced ferroptosis and improved liver regeneration, potentially through modulation of PPARα-related signaling, warranting further validation.
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JOURNAL OF ETHNOPHARMACOLOGY
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2025
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IF 5.4
Luoning Zhang,Tianyun Han,Rui Qian,Yao Xiao,Wen Zhu,Linshen Xie
Ethnopharmacological relevance Cadmium (Cd) can first damage the kidney, leading to renal tubular dysfunction and irreversible renal damage. Ganoderma lucidum is a traditional Chinese herb that can enhances kidney qi and is extensively used in the management of renal diseases. As a new type of high-quality Ganoderma lucidum , Ganoderma leucocontextum (GL) has been shown to have antioxidant, anti-apoptotic, and anti-inflammatory properties, demonstrating significant potential for application in the treatment of cadmium-toxic nephropathy Aim of the study This study intends to investigate the impact and mechanism of GL extract on cadmium-toxic nephropathy Materials and methods A mouse Cd-toxic nephropathy model was established by intragastric administration of cadmium chloride for 4 weeks. Serum was collected for renal function index detection, and renal tissue was collected for Cd content, histopathology, oxidative stress index, apoptosis, and autophagy index detection to evaluate the damage of renal function and the intervention effect of the extract. The chemical ingredients of the extracts were detected by ultra-high liquid chromatography coupled with mass spectrometry detection (UPLC-MS/MS), and the total antioxidant capacity was determined. The targets and pathways of interest were derived from the integration of transcriptomic and network pharmacology results. Western blot (WB) and quantitative real-time PCR (qPCR) were used for subsequent validation. Results GL extract effectively improved kidney damage caused by Cd-toxic nephropathy, especially the GL ethanol extract (GLE). Compared with the model group, the intervention group exhibited a significant reduction in serum creatinine (Scr) and blood urea nitrogen (BUN) levels, an enhancement in histopathological integrity, a notable decrease in malondialdehyde levels, a significant increase in glutathione levels and superoxide dismutase activity, as well as a marked elevation in the ratios of Bcl-2/Bax and LC3BⅡ/LC3BⅠ. Expression of Cleaved Caspase-3 and P62 protein was markedly reduced. Comprehensive network pharmacology and transcriptomic analysis showed that the AMPK signaling pathway is a crucial pathway, and PPARα is an important target and downstream regulator of the AMPK pathway. WB and qPCR analyses showed that the activation of AMPK, SIRT1, PGC-1α, and PPARα in the kidney tissue of mice in the model group was markedly diminished, whereas it was dramatically elevated following GLE intervention Conclusions GL extract can effectively ameliorate kidney damage caused by Cd accumulation, most likely through the AMPK/SIRT1/PGC-1α/PPARα signaling pathway.
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MOLECULAR CANCER RESEARCH
·
2022
·Vol. 20
·期 5
·810-822
·
IF 6.333
Ding Ming,Zhang Shuwei,Guo Yajuan,Yao Jingjing,Shen Qinghong,Huang Min,Chen Wenbo,Yu Shaofang,Zheng Yaqiu,Lin Yuefang,Yan Wenxin,Liu Zhongqiu,Su Tao,Lu Linlin
Acidification is recognized as the predominant characteristic of the tumor microenvironment (TME) and contributes to tumor progression. However, the mechanism of extracellular acidic TME directly influences intercellular pathologic responses remains unclear. Meanwhile, acidic TME is mainly ascribed to aberrant metabolism of lipids and glucose, but whether and how acidity affects metabolic reprogramming, especially for lipid metabolism, is still unknown. We found that lipid was significantly accumulated in liver cancer cells when exposed to acidic TME. Moreover, proteomic analysis showed that differentially expressed proteins were mainly clustered into fatty acid pathways. Subsequently, we found that acidification increased the expression of SCD1 by activating PI3K/AKT signaling pathway. Interestingly, we found that SCD1 directly bound to PPARα in the acidic TME, which vanished after 2-day reverse incubation in pH 7.4 medium, implying extracellular acidosis might influence intercellular function by mediating the binding affinity between SCD1 and PPARα under different pH gradients. In summary, our data revealed that acidosis could significantly trigger fatty acid synthesis to promote liver tumorigenesis by upregulating SCD1 in a PI3K/AKT activation dependent manner and simultaneously promote SCD1 binding to PPARα. Our study not only provides direct mechanistic evidence to support the vital role of acidosis in lipid metabolic reprogramming, but also provides novel insights for determining the binding affinity of functional proteins as a molecular mechanism to better understand the role of the acidic TME in tumor development. Implications: The acidic TME contributes to lipid accumulation in liver cancer by activating the PI3K/AKT signaling pathway and promoting SCD1–PPARα binding.
研究领域:
癌症生物学
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分子生物学
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细胞生物学
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生物化学
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Frontiers in Endocrinology
·
2023
·
IF 5.2
Tingwan Du,Lian Xiang,Jingjing Zhang,Chunmei Yang,Wenxin Zhao,Jialu Li,Yong Zhou,Ling Ma
Introduction The study aimed to explore the association of serum 25(OH)D 3 and hepatic steatosis in non-alcoholic fatty liver disease (NAFLD) patients and to determine whether the effect of vitamin D (VD) is mediated by activation of the peroxisome proliferator-activated receptor α (PPARα) pathway. Methods The study contained a case-control study, in vivo and in vitro experiments. A case-control study was conducted to compare serum parameters between NAFLD patients and controls and to evaluate the association of 25(OH)D 3 and NAFLD. In vivo study, male Wistar rats were randomly divided into control and model groups, fed a standard chow diet and a high-fat diet (HFD), respectively, for 7 weeks to generate an NAFLD model. Then, the rats were treated with VD and a PPARα antagonist (MK886) for 7 weeks. Tissue and serum were collected and assessed by biochemical assays, morphological analysis, histological analysis, and western blot analysis. In vitro , HepG2 cells were incubated with oleic acid (OA) to induce steatosis, which was evaluated by staining. HepG2 cells were pretreated with MK886 followed by calcitriol treatment, and differences in lipid metabolism-related proteins were detected by western blot. Results NAFLD patients were characterized by impaired liver function, dyslipidemia, and insulin resistance. Serum 25(OH)D 3 was negatively associated with alanine aminotransferase (ALT) in NAFLD. VD deficiency was a risk factor for patients with no advanced fibrosis. Adequate VD status (25(OH)D 3 >20 ng/mL) had a protective effect in patients after adjustment for confounding variables. NAFLD rats showed hyperlipidemia with severe hepatic steatosis, systematic inflammation, and lower serum 25(OH)D 3 . VD treatment ameliorated hepatic steatosis both in NAFLD rats and OA-induced HepG2 cells. Further, MK886 inhibited the anti-steatosis effect of VD. Conclusion The study revealed that an adequate VD level may act as a protective factor in NAFLD and that VD may alleviate hepatic steatosis via the PPARα signaling pathway.
研究领域:
肝病学
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内分泌学
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营养学
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分子生物学
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PHYTOMEDICINE
·
2026
·
IF 8.3
Wen Yan,Ying Huang,Yanjie Zhou,Qingfang Xie,Wanbin Huang,Yuexiu Lei,Zheman Xiao
Background Migraine is a common neurological disorder characterized by repeated attacks, with central sensitization recognized as a critical mechanism underlying the pathogenesis of chronic migraine (CM). Xanthohumol (Xn), a predominant bioactive allyl flavonoid derived from hops ( Humulus lupulus L. ), demonstrates notable anti-inflammatory and antioxidant properties. However, its therapeutic potential for migraine remains poorly characterized. Purpose The study focused on investigating the protective effects of Xn on a migraine model in mice, which was triggered by repeated dural applications of inflammatory soup (IS), and aimed to identify the underlying mechanisms. Methods A migraine mouse model was established through repeated dural IS stimulation. These mice received two doses of Xn treatment. Headache behavior was assessed using tests including head scratching, the periorbital mechanical threshold, cold allodynia, and light aversive behavior. Analyses of biomarkers and key protein expression via Western blot (WB), immunofluorescence (IF), and immunohistochemistry (IHC) were conducted to evaluate central sensitization. Through network pharmacology, molecular docking, cellular thermal shift assay (CETSA), and surface plasmon resonance (SPR), peroxisome proliferator-activated receptor α (PPARα) was identified as a potential target for Xn's migraine treatment. Downstream molecular mechanisms were validated by both activating and inhibiting PPARα. Results Comprehensive behavioral analyses revealed that Xn administration significantly alleviated migraine-like symptoms in migraine model mice, including increasing the periorbital mechanical threshold, reducing cold allodynia and head scratching, and improving light aversive behaviors. Network pharmacological analyses suggested that PPARα was a potential target for Xn in the treatment of migraine. Molecular docking, CETSA, and SPR experiments confirmed direct binding between Xn and PPARα. Mechanistic investigations demonstrated that Xn exerted regulatory effects through PPARα/AMPK pathway activation coupled with cyclooxygenase-2 (COX-2) suppression and downregulation of pro-inflammatory cytokines. Conclusion This study revealed that Xn alleviated migraine-related central censitization by activating the PPARα/AMPK axis and reducing neuroinflammation, proposing Xn as a novel migraine treatment.
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PHYTOTHERAPY RESEARCH
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2026
·
IF 8.1
Jianmei Zheng,Lu Cheng,Yingmin Wei,Mingshi Ren,Lei Wang,Jingwen Wang,Wuliu Zhou,Hui Huang,Feihua Wu
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent chronic liver disorder with limited treatment and manifests as hepatic lipid accumulation. The reduction of nuclear receptor corepressor 1 (NCoR1) activates the nuclear receptor PPARα, which plays a crucial role in alleviating lipid accumulation. We found that Scutellarin (Scu) regulated autophagy-mediated NCoR1/PPARα to enhance fatty acid (FA) β-oxidation and peroxisome production, thereby alleviating the lipid accumulation of MASLD. We used palmitic acid (PA)-treated human hepatocellular carcinoma (HepG2) and alpha mouse liver 12 (AML12) cells, as well as high-fat diet-fed C57BL/6J mice to evaluate the protective effect of Scu on MASLD. Scu reduced the levels of total cholesterol, triglycerides, and lipid droplets, whereas it dose-dependently increased the levels of β-hydroxybutyrate. In addition, Scu increased mRNA and protein expression of PPARα and promoted the transcriptional activity of FA β-oxidation-related target genes. In vitro, inhibition of PPARα with small interfering RNA (siRNA) abolished the activation of FA β-oxidation by Scu. Cellular thermal shift assay and drug affinity responsive target stability demonstrated that Scu did not interact directly with PPARα. Moreover, Scu increased the protein expression of 70-kDa peroxisomal membrane protein and the mRNA expression of peroxisome biogenesis-related genes. These effects were reversed by PPARα-siRNA. Scu improved the impaired autophagy while reducing the mRNA and protein expression of NCoR1. Notably, Scu reduced the colocalization of NCoR1 with PPARα and increased its colocalization with the autophagosome GABARAP. 3-MA, an autophagy inhibitor, attenuated Scu-mediated protective effects by FA β-oxidation and peroxisome biogenesis both in vitro and in vivo. In summary, Scu reduces lipid accumulation by improving the impaired autophagy, decreasing NCoR1 expression to activate PPARα, thereby simultaneously enhancing FA β-oxidation and peroxisome biogenesis, ultimately ameliorating hepatic steatosis.
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JOURNAL OF NUTRITIONAL BIOCHEMISTRY
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2025
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IF 4.9
Bing Li,Pengjun Zhong,Xueling Zhang,Chengguo Li,Min Luan,Yanlin Chen,Lei Chen,Wu Li,Rihui Wu
Metabolic dysfunction-associated steatotic liver disease (MASLD) represents a progressively critical global health concern, with no pharmacological interventions currently approved. Ursodeoxycholic acid (UDCA), an endogenous bile acid utilized in clinical practice, has demonstrated therapeutic potential in treating MASLD. However, the precise mechanisms by which UDCA exerts its hepatoprotective effects in MASLD remain to be fully characterized. We found that UDCA intervention markedly alleviated HFD-induced phenotypes, including hepatic steatosis, inflammation and metabolic disturbances, in high-fat diet (HFD)-fed mice. Mechanistically, UDCA treatment significantly activated hepatic peroxisome proliferator-activated receptor α (PPARα) and Cytochrome P450 family 4 subfamily A member 14 (CYP4A14)-mediated β-fatty acid oxidation. In vitro , treatment with UDCA effectively reduced lipid accumulation and liver enzyme release in AML12 hepatocytes subjected to palmitic acid (PA) and oleic acid (OA) challenge. UDCA administration significantly activated the PPARα-CYP4A14 signaling pathway, however, siRNA-mediated knockdown of these components resulted in a significant reduction of UDCA's protective efficacy in alleviating lipid accumulation in PA/OA-induced cellular models. Additionally, molecular docking and molecular dynamics simulations demonstrated stable interactions between UDCA and CYP4A14, indicating that UDCA may directly regulate CYP4A14 signaling. In conclusion, this study elucidates the CYP4A14-involved PPARα signaling as a novel mechanism by which UDCA exerts its anti-MASLD effects, thereby providing a theoretical foundation for considering UDCA as a potential therapeutic agent for MASLD.
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JOURNAL OF NATURAL PRODUCTS
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2022
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IF 4.803
Yichen Tong,Wentao Zhu,Tianzhi Wen,Zere Mukhamejanova,Fang Xu,Qi Xiang,Jiyan Pang
Nonalcoholic fatty liver disease (NAFLD) represents a class of disorders including hepatic steatosis, steatohepatitis, and liver fibrosis. Previous research suggested that xyloketal B (Xyl-B), a marine-derived natural product, could attenuate the NAFLD-related lipid accumulation. Herein, we investigated the protective mechanism of Xyl-B in a high-fat diet (HFD) mice fatty liver model by combining a quantitative proteomic approach with experimental methods. The results showed that the administration of Xyl-B (20 and 40 mg·kg–1·day–1, ip) ameliorated the hepatic steatosis in HFD mice. Proteomic profiling together with bioinformatics analysis highlighted the upregulation of a cluster of peroxisome proliferator-activated receptor-α (PPARα) downstream enzymes mainly related to fatty acid oxidation (FAO) as key changes after the treatment. These changes were subsequently confirmed by bioassays. Moreover, further results showed that the expression levels of PPARα and PPARγ coactivator-1α (PGC1α) were increased after the treatment. The related mode-of-action was confirmed by PPARα inhibition. Furthermore, we evaluated the PPARα-mediated anti-inflammatory and antifibrosis effect of Xyl-B in methionine-choline-deficient (MCD) mice hepatitis and liver fibrosis models. According to the results, the histological features were improved, and the levels of inflammatory factors, adhesion molecules, as well as fibrosis markers were decreased after the treatment. Collectively, these results indicated that Xyl-B ameliorated different phases of NAFLD through activation of the PPARα/PGC1α signaling pathway. Our findings revealed the possible metabolism-regulating mechanism of Xyl-B, broadened the application of xyloketal family compounds, and may provide a new strategy to curb the development of NAFLD.
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DRUG METABOLISM AND DISPOSITION
·
2022
·Vol. 50
·期 12
·1464-1471
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IF 3.579
Jie Yang,Shicheng Fan,Yifei Zhang,Min Huang,Yue Gao,Huichang Bi
Peroxisome proliferator-activated receptor α (PPARα) is closely related to lipid metabolism and various liver diseases. Previous study has shown that chronic treatment with PPARα agonist WY-14643 can induce liver tumors in rodents, but the implications of this process on lipid metabolism in the liver remain unclear. Thus, this study aimed to explore the influences of chronic treatment with WY-14643 on the liver and hepatic lipid metabolism. Wild-type C57BL/6 mice were treated with WY-14643 (100 mg/kg/week, i.p.) or corn oil, and liver and serum samples were collected for testing after 42 weeks of WY-14643 treatment. The results showed that hepatomegaly, liver tumors with mild liver injury, and hepatocyte proliferation were induced in mice treated with WY-14643. The mRNA and protein expression levels of PPARα downstream targets acyl-CoA oxidase 1 and cytochrome P450 4A were significantly upregulated in the WY-14643–treated group. Lipidomic analysis revealed that chronic treatment with WY-14643 disturbed lipid homeostasis, especially triglycerides (TGs), which were significantly elevated after WY-14643 treatment. Moreover, TG homeostasis-related genes were significantly increased in the WY-14643–treated group. In conclusion, these findings demonstrated that hepatomegaly and liver tumors induced by chronic treatment with WY-14643 in mice are accompanied by hepatocyte proliferation and TG accumulation.
研究领域:
药理学
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肝病学
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分子生物学
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