Communications Biology
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2025
·Vol. 8
·期 1
·1-16
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IF 5.1
Bie Pengfei,Su Dongpo,Gao Yang,Wu Liang,Niu Zhanfeng,Zhao Yanbin,He He,Jiang Zhanfeng,Zeng Zhong,Zhang Yaolin,Fan Heng,Xia Hechun
Microglia play significant roles in spinal cord injury (SCI) progression. Previous studies have suggested that ferroptosis plays a crucial role in exacerbating neuronal death following SCI; however, the role of microglial ferroptosis in SCI and the underlying mechanisms remain elusive. Here, we elucidate that lipid droplets accumulate in microglia to facilitate microglial ferroptosis after SCI. Notably, microglial ferroptosis peaks at 3 days post-injury, after which it decreases. Microglial Period 2 (Per2) expression is elevated after SCI in vivo; this change is highly synchronized with the changes in microglial ferroptosis. Microglia-specific Per2 knockout promoted neurological function recovery by suppressing microglial ferroptosis. In vitro, Per2 overexpression and deficiency amplified and mitigated microglial ferroptosis, respectively. RNA-seq indicated that Gpx4 was downregulated by Per2. Coimmunoprecipitation demonstrated that Per2 directly interacted with PPARα. Overall, our results indicate that Per2 determines the susceptibility of microglial ferroptosis via the PPARα-Gpx4 axis after SCI.
研究领域:
神经科学
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细胞生物学
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分子生物学
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免疫学
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高影响因子
PHYTOMEDICINE
·
2023
·
IF 7.9
Qian Li,Wen Zhang,Nuo Cheng,Yadi Zhu,Hao Li,Shuijun Zhang,Wenzhi Guo,Guangbo Ge
Background Cirsii Japonici Herba Carbonisata (Dajitan in Chinese) has been used to treat liver disorders in Asian countries. Pectolinarigenin (PEC), an abundant constituent in Dajitan, has been found to possess a wide range of biological benefits, including hepatoprotective effects. However, the effects of PEC on acetaminophen (APAP)-induced liver injury (AILI) and the underlying mechanisms have not been studied. Purposes To explore the role and mechanisms of PEC in protecting against AILI. Study design and methods The hepatoprotective benefits of PEC were studied using a mouse model and HepG2 cells. PEC was tested for its effects by injecting it intraperitoneally before APAP administration. To assess liver damage, histological and biochemical tests were performed. The levels of inflammatory factors in the liver were measured using RT-PCR and ELISA . Western blotting was used to measure the expression of a panel of key proteins involved in APAP metabolism, as well as Nrf2 and PPARα. PEC mechanisms on AILI were investigated using HepG2 cells, while the Nrf2 inhibitor (ML385) and PPARα inhibitor (GW6471) were used to validate the importance of either Nrf2 and PPARα in the hepatoprotective effects of PEC. Results PEC treatment decreased serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) levels in the liver. PEC pretreatment increased the activity of superoxide dismutase (SOD) and glutathione (GSH) while decreasing malondialdehyde production (MDA). PEC could also up-regulate two important APAP detoxification enzymes (UGT1A1 and SULT1A1). Further research revealed that PEC reduced hepatic oxidative damage and inflammation, and up-regulated APAP detoxification enzymes in hepatocytes by activating the Nrf2 and PPARα signaling pathways . Conclusions PEC ameliorates AILI by decreasing hepatic oxidative stress and inflammation while increasing phase Ⅱ detoxification enzymes related to APAP harmless metabolism through activation of Nrf2 and PPARα signaling. Hence, PEC may serve as a promising therapeutic drug against AILI.
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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毒理学
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PubMed
高影响因子
BIOORGANIC CHEMISTRY
·
2026
·
IF 5.1
Hui Li,Hengli Luo,Xin Zhang,Jianchun Luo,Chenglin Zhan,Xiaofang Gong,Minghua Liu,Xiangfeng Chen,Ge Zhao
Rhoifolin alleviated pathological and histological changes in DNCB-induced Balb/c mice with AD-like responses. • Rhoifolin suppressed pro-inflammatory chemokine and cytokine production in TNF-α/IFN-γ-stimulated HaCaT cells. • Rhoifolin regulated skin barrier function and inflammation via PPARα-mediated NF-κB/NLRP3 pyroptosis signaling. Rhoifolin (ROF), a naturally occurring flavonoid glycoside, has been documented to possess a broad spectrum of biological properties, including anticancer, antioxidant, neuroprotective, hepatoprotective, anti-inflammatory, and antiviral activities. Atopic dermatitis (AD) is a persistent, recurring inflammatory skin illness that frequently greatly compromises the patients' quality of life. Nevertheless, the role of ROF in AD pathogenesis and the associated molecular events have yet to be elucidated. Our findings revealed that ROF administration substantially ameliorated the 1-chloro-2,4-dinitrobenzene (DNCB)-induced AD-like phenotypes, as reflected by decreased mast cell accumulation, reduced CD4 + and CD8 + T cells infiltration within lesional skin, lowered serum immunoglobulin E (IgE) concentrations, attenuated epidermal and dermal thickening, suppressed histamine liberation and pruritic episodes, improved SCORAD indices, concomitant restoration of skin barrier protein expression, and curtailed the production of multiple inflammatory factors. Mechanistic investigations, integrating network pharmacology forecasts, transcriptomic profiling, and pharmacological blockade experiments with specific antagonists, further confirmed that the anti-inflammatory action of ROF operates through the PPARα-regulated NF-κB/NLRP3 signaling cascade. Collectively, these observations demonstrate that ROF exerts favorable inhibitory effects against AD-like inflammation both in vivo and in vitro , underscoring its potential as a viable therapeutic option for managing AD and other inflammatory cutaneous disorders. Download: Download high-res image (81KB) Download: Download full-size image
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Scientific Reports
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2025
·Vol. 15
·期 1
·1-19
·
IF 3.9
Liu Yunxiao,Wang Shuanghu,Younas Ayesha,Lv Jiaojian,Al Mamun Abdullah,Shao Chuxiao
Nonalcoholic Fatty Liver Disease (NAFLD) is characterized by excessive lipid accumulation in hepatocytes and is closely associated with metabolic disturbances such as obesity, dyslipidemia, and insulin resistance. Despite its increasing prevalence and potential progression to severe liver conditions, there is currently no approved pharmaceutical intervention for NAFLD. Traditional Chinese Medicine (TCM) formulations, such as Xiaoyao San (XYS), have shown therapeutic efficacy in treating NAFLD, but the underlying mechanisms remain unclear. This study employed a multi-omics approach to elucidate the therapeutic mechanisms of XYS in NAFLD. A rat model of NAFLD was established using a high-fat diet (HFD). The chemical constituents of XYS were analyzed using UPLC-MS/MS. Transcriptomics and proteomics analyses were performed to identify potential biological targets and signaling pathways involved in the therapeutic effects of XYS. The results were validated using ELISA and Western blotting. UPLC-MS/MS identified 225 prototype chemical components of XYS in the blood. XYS significantly reduced body weight, liver index, and Lee’s index in NAFLD model rats. It ameliorated HFD-induced hepatic steatosis, down-regulated serum levels of ALT, AST, GGT, TG, TC, LDL-C, FBG, IL-1β, IL-6, TNF-α, and ROS, and up-regulated HDL-C levels. Transcriptomics and proteomics analyses revealed that XYS modulated key signaling pathways, including cAMP, TGF-β, NF-κB, and necroptosis. Specifically, XYS down-regulated the expressions of NF-κB, p-NF-κB, FOXO1, TGF-β1, RIP3, and p-MLKL, while up-regulating cAMP, PKA, p-PKA, and PPARα. XYS improves NAFLD by regulating the cAMP/PKA-mediated PPARα, FOXO1, and NF-κB signaling pathways. This study provides a comprehensive understanding of the molecular mechanisms underlying the therapeutic effects of XYS in NAFLD and supports its potential as a novel therapeutic intervention for this condition.
研究领域:
药理学
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代谢疾病
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系统生物学
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高影响因子
DRUG METABOLISM AND DISPOSITION
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2019
·Vol. 47
·期 6
·582-591
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IF 3.354
Mengru Bai,Qingquan Zeng,Yingchun Chen,Mingyang Chen,Ping Li,Zhiyuan Ma,Dongli Sun,Hui Zhou,Caihong Zheng,Su Zeng,Huidi Jiang
l-Carnitine (l-Car) plays a crucial role in fatty acid β-oxidation. However, the plasma l-Car concentration in women markedly declines during pregnancy, but the underlying mechanism and its consequences on maternal hepatic β-oxidation have not yet been clarified. Our results showed that the plasma l-Car level in mice at gestation day (GD) 18 was significantly lower than that in nonpregnant mice, and the mean fetal-to-maternal plasma l-Car ratio in GD 18 mice was 3.0. Carnitine/organic cation transporter 2 (OCTN2) was highly expressed in mouse and human placenta and upregulated as gestation proceeds in human placenta, whereas expressions of carnitine transporter (CT) 1, CT2, and amino acid transporter B0,+ were extremely low. Further study revealed that renal peroxisome proliferator–activated receptor α (PPARα) and OCTN2 were downregulated and the renal l-Car level was reduced, whereas the urinary excretion of l-Car was lower in late pregnant mice than in nonpregnant mice. Meanwhile, progesterone (pregnancy-related hormone) downregulated the expression of renal OCTN2 via PPARα-mediated pathway, and inhibited the activity of OCTN2, but estradiol, corticosterone, and cortisol did not. Unexpectedly, the maternal hepatic level of l-Car and β-hydroxybutyrate (an indicator of mitochondrial β-oxidation), and mRNA levels of several enzymes involved in fatty acid β-oxidation in GD 18 mice were higher than that in nonpregnant mice. In conclusion, OCTN2 mediated l-Car transfer across the placenta played a major role in maternal plasma l-Car reduction during pregnancy, which did not subsequently result in maternal hepatic fatty acid β-oxidation decrease.
研究领域:
生理学
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药理学
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内分泌学
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生殖生物学
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分子生物学
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高影响因子
PHYTOMEDICINE
·
2026
·
IF 11.3
Xiangyu Cai,Zhaoyu Yang,Yingyu Xiao,Qiongyu Yuan,Wanyue Gao,Jing Dong,Weidong Zeng,Yuling Mi,Caiqiao Zhang
Background Ovarian aging is characterized by progressive impairments of follicular development and reproductive performance. Increasing evidence indicates that metabolic dysregulation plays a central role in the decline of ovarian function. Chlorogenic acid (CGA), a widely distributed plant-derived polyphenol, is known for its antioxidant, anti-inflammatory, and metabolic properties. However, its potential role in ovarian aging and the underlying mechanisms remain unexplored. Methods D-galactose-induced granulosa cell (GC) senescence model and naturally aging laying chickens were used for evaluating the protective effects of CGA on ovarian aging. Cellular senescence, mitochondrial function, lipid metabolism, and steroidogenic capacity were evaluated through molecular, biochemical, transcriptomic, and histological analyses. Mechanistic studies employed pharmacological inhibition and genetic knockdown to delineate the signaling hierarchy. Results In D-gal-induced GCs, CGA mitigated cellular senescence, improved mitochondrial function, and restored key steroidogenic gene expression ( STAR, CYP11A1 , and CYP19A1 ). Mechanistically, CGA reversed metabolic dysregulation by suppressing ERK1/2 phosphorylation to restore PPARα activity. This mechanism was supported by pharmacological ERK1/2 inhibition, which amplified these benefits, and siRNA-mediated PPARα silencing, which blunted CGA-induced steroidogenic recovery. In naturally aging laying chickens, CGA supplementation enhanced serum estradiol and antioxidant capacity. Crucially, CGA positively modulated the liver-ovary axis by rejuvenating hepatic lipid metabolism and systemic transport, thereby promoting yolk deposition, follicular development, and egg-laying performance. Conclusion These findings suggest that CGA mitigates ovarian aging by coordinating mitochondrial homeostasis, lipid metabolism, and steroidogenesis via the ERK/PPARα pathway. The result provides mechanistic insight into the potential of plant-derived polyphenols as metabolic regulators for preserving ovarian function.
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Chinese Journal of Integrative Medicine
·
2025
·
IF 2.5
Liu Shu-yan,Zhang Xiao-wei,Gao Gai,Liu Chang-xin,Chen Hui,Fu Zhong-xue,Xu Jiang-yan,Wang Zhen-zhen,Zhang Zhen-qiang,Xie Zhi-shen
Objective To investigate the therapeutic potential of pseudolaric acid B (PAB) on non-alcoholic fatty liver disease (NAFLD) and its underlying molecular mechanism in vitro and in vivo . Methods Eight-week-old male C57BL/6J mice ( n =32) were fed either a normal chow diet (NCD) or a high-fat diet (HFD) for 8 weeks. The HFD mice were divided into 3 groups according to a simple random method, including HFD, PAB low-dose [10 mg/(kg·d), PAB-L], and PAB high-dose [20 mg/(kg·d), PAB-H] groups. After 8 weeks of treatment, glucose metabolism and insulin resistance were assessed by oral glucose tolerance test (OGTT) and insulin tolerance test (ITT). Biochemical assays were used to measure the serum and cellular levels of total cholesterol (TC), triglycerides (TG), aspartate aminotransferase (AST), alanine aminotransferase (ALT), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C). White adipose tissue (WAT), brown adipose tissue (BAT) and liver tissue were subjected to hematoxylin and eosin (H&E) staining or Oil Red O staining to observe the alterations in adipose tissue and liver injury. PharmMapper and DisGeNet were used to predict the NAFLD-related PAB targets. Peroxisome proliferator-activated receptor alpha (PPARα) pathway involvement was suggested by Kyoto Encyclopedia of Genes and Genomes (KEGG) and search tool Retrieval of Interacting Genes (STRING) analyses. Luciferase reporter assay, cellular thermal shift assay (CETSA), and drug affinity responsive target stability assay (DARTS) were conducted to confirm direct binding of PAB with PPARα. Molecular dynamics simulations were applied to further validate target engagement. RT-qPCR and Western blot were performed to assess the downstream genes and proteins expression, and validated by PPARα inhibitor MK886. Results PAB significantly reduced serum TC, TG, LDL-C, AST, and ALT levels, and increased HDL-C level in HFD mice ( P <0.01). Target prediction analysis indicated a significant correlation between PAB and PPARα pathway. PAB direct target binding with PPARα was confirmed through luciferase reporter assay, CETSA, and DARTS ( P <0.05 or P <0.01). The target engagement between PAB and PPARα protein was further confirmed by molecular dynamics simulations and the top 3 amino acid residues, LEU321, MET355, and PHE273 showed the most significant changes in mutational energy. Subsequently, PAB upregulated the genes expressions involved in lipid metabolism and mitochondrial biogenesis downstream of PPARα ( P <0.05 or P <0.01). Significantly, the PPARα inhibitor MK886 effectively reversed the lipid-lowering and PPARα activation properties of PAB ( P <0.05 or P <0.01). Conclusion PAB mitigates lipid accumulation, ameliorates liver damage, and improves mitochondrial biogenesis by binding with PPARα, thus presenting a potential candidate for pharmaceutical development in the treatment of NAFLD.
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CARBOHYDRATE POLYMERS
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2026
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IF 13.2
Lanjia Ao,Yujie Li,Lingling Zheng,Xiaolin Chen,Haoyuan Zeng,Wen Miao,Shuxian Yang,Tingting Zhou,Na Li,Jian-Lin Wu
Bioactive pectin is a considerable candidate for drug delivery to improve stability and bioavailability. Geniposide (GS) is a hepatoprotective compound with poor bioavailability, limiting its application. Herein, we first designed a self-assembled Gardenia Pectin Gel (GPG) from pectin-rich Gardenia jasminoides Ellis fruit extracts (GE), spontaneously encapsulating co-extracted GS. Compared with non-gelling GE, pectin gel delivery achieved enhanced stability and delayed release in vitro and increased half-time (2.6-fold, p < 0.05) and bioavailability (2.35-fold, p < 0.05) of GS in vivo. Moreover, GPG provided superior hepatoprotective effects over GS and GE, including reducing hepatic injury indicators (e.g. ALP level, p < 0.01 vs GS; p < 0.05 vs GE), inflammation and necrosis in α-naphthylisothiocyanate-induced cholestatic liver disease (CLD) mice. Mechanistically, GPG restored hepatic glycolipid metabolic homeostasis via GS-mediated PPARα activation. Meanwhile, GPG promoted gut microbes remodeling and hepatoprotective acetate and butyrate production ( p < 0.001), producing synergistic effects. Notably, after 7-day administration, GPG outperformed ursodeoxycholic acid, a first-line CLD medicine, in the CLD mice model, demonstrating its clinical potential. Collectively, this study developed a promising self-assembled pectin-assisted formulation that enhanced the bioavailability of GS and CLD intervention, more importantly, established a theoretical foundation for clinical application of pectin-based drug delivery systems.
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Journal of Future Foods
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2026
·
IF 10.6
Bailin Li,Fen Liu,Yaoguang Huang,Sui Kiat Chang,Chenqi Niu,Pu Liu,Xiancai Li,Liyuan Yao,Sheng-Xiang Qiu
Pigeon pea ( Cajanus cajan (L.) Millsp.), a plant with documented safety and dual use in food and traditional medicine, holds promise for developing hepatoprotective agents. This study aimed to evaluate its potential to mitigate high-fat diet (HFD)-induced hepatic steatosis. We investigated a stilbene-enriched extract (EX) from pigeon pea leaves and its major constituent, cajanstilbenoid A (CSA). In HFD-fed mice, both EX and CSA significantly reduced body weight, liver index, lipid accumulation and serum cholesterol/triglyceride levels. CSA also ameliorated oxidative stress and improved liver function markers. Mechanistic studies revealed that CSA acted as a selective agonist of peroxisome proliferator-activated receptor alpha (PPARα): Network pharmacology, transcriptomics, and molecular docking predicted PPARα as a target; this was confirmed by cellular thermal shift assay (CETSA), drug affinity responsive target stability assays (DARTS) and surface plasmon resonance (SPR), which demonstrated direct binding. Crucially, siRNA-mediated knockdown of PPARα in HepG2 cells abolished the lipid-lowering effects of CSA. Our findings demonstrated that CSA alleviated HFD-induced hepatic steatosis primarily by activating the PPARα pathway, reducing oxidative stress and promoting lipid metabolism. This study highlighted the therapeutic potential of CSA for non-alcoholic fatty liver disease and underscored pigeon pea as a valuable medicinal and edible resource.
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PeerJ
·
2020
·
IF 2.379
Xiaoyan Li,Yiyan Lu,Xiaojun Ou,Sijing Zeng,Ying Wang,Xiaoxiao Qi,Lijun Zhu,Zhongqiu Liu
Background This study aimed to systematically profile the alterations and sex- and age-related differences in the drug metabolizing enzymes (DMEs) in a KRAS-mutant mouse model of lung cancer (KRAS mice). Methodology In this study, the LC-MS/MS approach and a probe substrate method were used to detect the alterations in 21 isoforms of DMEs, as well as the enzymatic activities of five isoforms, respectively. Western blotting was applied to study the protein expression of four related receptors. Results The proteins contents of CYP2C29 and CYP3A11, were significantly downregulated in the livers of male KRAS mice at 26 weeks (3.7- and 4.4-fold, respectively, p < 0.05). SULT1A1 and SULT1D1 were upregulated by 1.8- to 7.0- fold at 20 ( p = 0.015 and 0.017, respectively) and 26 weeks ( p = 0.055 and 0.031, respectively). There were positive correlations between protein expression and enzyme activity for CYP2E1, UGT1A9, SULT1A1 and SULT1D1 ( r 2 ≥ 0.5, p < 0.001). Western blotting analysis revealed the downregulation of AHR, FXR and PPARα protein expression in male KRAS mice at 26 weeks. For sex-related differences, CYP2E1 was male-predominant and UGT1A2 was female-predominant in the kidney. UGT1A1 and UGT1A5 expression was female-predominant, whereas UGT2B1 exhibited male-predominant expression in liver tissue. For the tissue distribution of DMEs, 21 subtypes of DMEs were all expressed in liver tissue. In the intestine, the expression levels of CYP2C29, CYP27A1, UGT1A2, 1A5, 1A6a, 1A9, 2B1, 2B5 and 2B36 were under the limitation of quantification. The subtypes of CYP7A1, 1B1, 2E1 and UGT1A1, 2A3, 2B34 were detected in kidney tissue. Conclusions This study, for the first time, unveils the variations and sex- and age-related differences in DMEs in C57 BL/6 (WT) mice and KRAS mice.
研究领域:
药理学
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肿瘤学
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分子生物学
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高影响因子
Chinese Herbal Medicines
·
2024
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IF 4.7
Shuang He,Xiaoling Liang,Weixiong Chen,Yangji Nima,Yi Li,Zihui Gu,Siyue Lai,Fei Zhong,Caixiong Qiu,Yuying Mo,Jiajun Tang,Guanyi Wu
Objective This study aims to elucidate the therapeutic potential of osthole for the treatment of atopic dermatitis (AD), focusing on its ability to alleviate chronic pruritus (CP) and the underlying molecular mechanisms. Methods In this study, we investigated the anti-inflammatory effects of osthole in both a 2,4-dichloronitrobenzene (DNCB)-induced AD mouse model and tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) stimulated human immortalized epidermal (HaCaT) cells. The anti-itch effect of osthole was specifically assessed in the AD mouse model. Using methods such as hematoxylin and eosin (HE) staining, enzyme-linked immunosorbent assay (ELISA), western blot (WB), quantitative real-time PCR (qRT-PCR), and immunofluorescence staining. Results Osthole improved skin damage and clinical dermatitis scores, reduced scratching bouts, and decreased epidermal thickness in AD-like mice. It also reduced the levels of interleukin (IL)-31 and IL-31 receptor A (IL-31 RA) in both skin tissues and HaCaT cells. Furthermore, Osthole suppressed the protein expression levels of phosphor-p65 (p-p65) and phosphor-inhibitor of nuclear factor kappa-Bα (p-IκBα). Meanwhile, it increased the protein expression levels of peroxisome proliferator-activated receptor α (PPARα) and PPARγ in HaCaT cells. Conclusion These findings indicated that osthole effectively inhibited CP in AD by activating PPARα, PPARγ, repressing the NF-κB signaling pathway, as well as the expression of IL-31 and IL-31 RA.
研究领域:
药理学
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免疫学
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皮肤病学
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高影响因子
CELLULAR AND MOLECULAR LIFE SCIENCES
·
2025
·Vol. 82
·期 1
·1-17
·
IF 6.2
Zhong Chong-Chao,Zhang Xu,Pantopoulos Kostas,Song Chang-Chun,Yang Hong,Wei Xiao-Lei,Luo Zhi
Copper (Cu) and zinc (Zn) are essential trace elements for terrestrial animals. Studies suggested that single dietary Cu- or Zn- deficiency lead to liver lipid deposition and cause metabolic dysfunction-associated steatotic liver disease (MASLD). However, the mechanisms by which dietary Cu and Zn co-deficiency promote hepatic lipid deposition and metabolism remain unknown. Our study found that, compared to single Cu- or Zn- deficiency, Cu and Zn co-deficiency significantly increased lipid deposition, induced mitochondrial oxidative stress, disrupted mitochondrial structure and function, and inhibited lipolysis in hepatocytes and whole liver tissue. Mechanistically, Cu and Zn co-deficiency-induced lipotoxicity was mediated by sirtuin 3 (Sirt3). Sirt3 inhibited the acetylation and degradation of forkhead box O3 (Foxo3), preventing its binding to the peroxisome proliferator-activated receptor alpha (PPARα) promoter, which accordingly increased lipid deposition. Overall, for the first time, we elucidated the mechanism by which Cu and Zn co-deficiency aggravates hepatic lipotoxicity and identified the critical regulatory role of the Sirt3/Foxo3/PPARα pathway during this process, with the fish as the model.
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