INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2025
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IF 8.5
Wenqian Wang,Qingfu Zhang,Tong Zhang,Fuping Lu,Fufeng Liu
Current therapeutic options for Parkinson's disease (PD) are limited in efficacy and burdened with severe side-effects. Inflammation, intertwined with oxidative stress and influenced by gut microbiota-related changes making the gut-brain axis the main target of innovative therapies. This study reveals the multiple protective effects of polysaccharides extracted from Ulva lactuca (UPE) on PD models. In vitro, UPE was shown to have direct cytoprotective effects, including mitigating 1-methyl-4-phenylpyridinium-induced cell apoptosis, reducing reactive oxygen species levels, and maintaining mitochondrial membrane potential. In vivo, oral UPE significantly restored motor deficits and dopaminergic neuron loss caused by MPTP. These in vivo benefits were associated with the inhibition of oxidative stress and inflammation. Moreover, oral UPE inhibits the excessive activation of glial cells and the excessive production of pro-inflammatory factors and oxidative stress markers in serum. Furthermore, 16S rRNA analysis of gut microbiota revealed that UPE reshaped the gut microbiota of PD mice by increasing the abundance of norank_f_Murbaculaceae and decreasing the abundance of Desulfovibrio . Mechanically, the Nrf2/HO-1 and TLR4/NF-κB signaling pathways are involved in the anti-PD effect of UPE. In general, UPE offers new perspectives on PD treatment and demonstrates the potential of natural polysaccharides in treating neurodegenerative diseases.
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PHYTOMEDICINE
·
2023
·
IF 7.9
Hongkang Zhu,Fanglin Shen,Xiaochen Wang,He Qian,Yu Liu
Background Sleep deprivation (SD) has become a global health concern with serious consequences containing memory deficits and gastrointestinal dysfunctions. The gut-brain axis serves as a crucial link between the brain and gut, and the utilization of chlorogenic acid (CGA) presents a compelling strategy for mitigating or potentially resolving various neuroinflammation-associated disorders. However, it is still unknown how CGA may interact with the gut, microbiota and the brain during SD. Purpose This study aims to explore the therapeutic effect and underlying mechanism of microbiota-gut-brain axis by which CGA prevents SD-induced cognitive deficits. Study design and methods CGA (30, 60 mg/kg.bw.) was gavaged to C57BL/6 mice, and then submitted to 48-h SD. The cognitive and spatial learning abilities were investigated through behavioral tests. Furthermore, we explored the action mechanism of this compound with haematological analysis, histopathological examination, Western blot, ELISA and 16S rRNA gene pyrosequencing from colonic contents. Results The cognitive deficits induced by SD were significantly relieved by administration of CGA in a dose-dependent manner. The H&E staining of hippocampus and colon tissues indicated that pretreatment of CGA not only protected brain tissue from SD, but also maintained intestinal integrity. In the hippocampus, the increased pro-inflammatory neurometabolites were significantly prevented by CGA, and an immune profile capable of hippocampal-dependent spatial memory was improved via Nrf2/PPAR signaling pathways. The observed immunomodulatory effect was concomitant with augmentation of the intestinal barrier, as evidenced by the heightened expressions of tight junction proteins. 16s rRNA analysis of colonic contents revealed that levels of Clostridia_UCG-014 and LPS were significantly inhibited, and those of Lactobacillus and intestinal tight junction proteins were upregulated in the CGA group. Pathways of ko05322 (immune disease) and ko04610 (immune system) were significantly regulated by CGA. Based on PICRUSt2 algorithm, CGA probably influenced gut microbial functions via several metabolism pathways, such as arginine biosynthesis, pyrimidine metabolism and purine metabolism. Conclusion The present study first proved the efficacy and mechanism of CGA in alleviating SD-induced cognitive impairment and neuroinflammatory via creating a systemic protection, a bidirectional communication system connecting the gut with the brain. The intestinal barrier improvement and the reshaped “SD microbiota” profiles restored immunity functions, which were the main contributors to Nrf2/PPAR activation and the neuroprotective effect of CGA. Overall, this work provided novel insights of CGA, which would guide the more reasonable clinical use of CGA in the pathogenesis of sleep-related disorders.
研究领域:
神经科学
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免疫学
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微生物学
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药理学
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分子生物学
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Foods
·
2024
·Vol. 13
·期 15
·2440
·
IF 4.7
Jingwen Yu,Xiangwei Xiao,Baiying Chen,Zeyuan Deng,Xuan Chen,Yawei Fan,Hongyan Li
The antioxidant activities of lycopene (LY), lutein (LU), chlorogenic acid (CA), and delphinidin (DP) were tested in vitro on H9c2 cell-based models. Some indicators, such as the generation of reactive oxygen (ROS), the quantification of cell antioxidant activity (CAA), and the expressions of SOD, GSH-Px, and CAT, were calculated to examine their antioxidant interactions. From our results, the phytochemical mixtures (M1: CA-LU: F3/10, M2: DP-CA: F7/10, M3: DP-LY: F5/10) displayed strong synergistic effects based on the generation of ROS and the quantification of CAA. However, great antagonistic bioactivities were seen in the combinations of LY-LU: F5/10 (M4), CA-LU: F9/10 (M5), and DP-LY: F7/10 (M6). Western blotting analysis indicated that the possible mechanism underlying the synergistic antioxidant interactions among phytochemical combinations was to enhance the accumulation of Nrf2 in the nucleus and the expression of its downstream antioxidant enzymes, HO-1 and GCLC. The combinations (M1–M3 groups) showed significant protection against the loss of mitochondrial membrane potential than individual groups to avoid excessive ROS production. The M4–M6 groups exerted antagonistic protective effects compared with the individual groups. In addition, lutein and lycopene absorption was improved more because of the presence of chlorogenic acid and delphinidin in the M1 and M3 groups, respectively. However, delphinidin significantly reduced the cellular uptake of lycopene in the M6 group. It appeared that antioxidant interactions of phytochemical combinations may contribute to the restoration of cellular redox homeostasis and lead to an improvement in diet quality and collocation.
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Food & Function
·
2018
·Vol. 9
·期 3
·1701-1712
·
IF 3.289
Shangkun Tang,Qian Tang,Jialei Jin,Gang Zheng,Jianchen Xu,Wu Huang,Xiaobin Li,Ping Shang,Haixiao Liu
Osteoarthritis (OA), which is characterized by progressive degradation of the articular cartilage, is the most prevalent form of human arthritis. Accumulating evidence has shown that polydatin (PD) exerts special biological functions in a variety of diseases. However, whether it protects against OA development has remained unknown. Here, we investigated the anti-inflammatory and chondroprotective effects of PD on interleukin (IL)-1β-induced human osteoarthritic chondrocytes and in the surgical destabilization of medial meniscus mouse (DMM) OA models. In vitro, PD treatment completely suppressed the over-production of pro-inflammatory mediators, including prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), nitric oxide (NO), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and IL-6 in IL-1β-induced human OA chondrocytes. Moreover, PD exerted a suppressive effect on the expression of matrix-degrading proteases, including matrix metalloproteinase 13 (MMP13) and thrombospondin motifs 5 (ADAMTS-5), which leads to the degradation of the extracellular matrix (ECM). Meanwhile, specific inhibition of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) level by short-interfering RNA (siRNA) strongly reversed the anti-inflammatory and chondroprotective effects of PD in human OA chondrocytes. The protective effects of PD were also observed in vivo. In conclusion, our studies demonstrate that PD holds novel therapeutic potential for the development of OA.
研究领域:
风湿病学
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药理学
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炎症
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骨科
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分子生物学
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JOURNAL OF ENVIRONMENTAL SCIENCE AND HEALTH PART A-TOXIC/HAZARDOUS SUBSTANCES & ENVIRONMENTAL ENGINEERING
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2026
·
IF 2
Jing Zhu,Mengmeng Gao,Hao Ling,Phar Ku Ngwe,Chengxiang Guo,Yinan Hu,Jicang Wang
This study investigated the protective effects of naringenin (Nar) against lead (Pb)-induced testicular injury in rats, focusing on the Nrf2/Keap1 antioxidant pathway and PINK1/Parkin-mediated mitophagy. To this end, male SD rats were exposed to Pb (60 mg/kg) and co-treated with Nar (50 mg/kg) for 8 consecutive weeks, followed by assessments via biochemical detection, oxidative stress (OS) evaluation, hematological examination, histopathological observation, qPCR, WB, and IHC analyses. Pb exposure caused hematological disturbances, reduced serum LH and T levels, and OS imbalance (lower GSH, SOD, CAT; higher MDA), aggravating testicular damage. Meanwhile, it suppressed the Nrf2/NQO1 pathway, elevated Keap1, impaired autophagy (elevated p62, declined LC3‑II/LC3‑I ratio), and induced aberrant accumulation of PINK1/Parkin. Co-treatment with Nar mitigated these alterations, ameliorating testicular injury, restoring redox homeostasis and serum reproductive hormone levels, and normalizing key molecular expressions in both pathways. In conclusion, Nar alleviates Pb-induced rat testicular damage by reactivating the Nrf2/Keap1 axis to suppress OS, and by restoring autophagic flux to facilitate PINK1/Parkin-mediated clearance of damaged mitochondria.
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CHEMICO-BIOLOGICAL INTERACTIONS
·
2026
·
IF 5.2
Hongchuang Ma,Nan Shen,Xin Liu,Fangfang Zhou,Chuanming Hao,Qun Luo
Background Acute kidney injury (AKI) remains a major clinical challenge lacking effective pharmacological interventions. Ferroptosis has emerged as a critical mechanism contributing to renal tubular injury. While p -coumaric acid (pCA), a natural phenolic compound, has been reported to exert renoprotective effects, its regulatory role in ferroptosis, particularly under different pathological contexts of AKI, remains incompletely understood. Methods A folic acid (FA, 250 mg/kg)–induced AKI model was established in mice treated with pCA (10 and 50 mg/kg). Renal function, histopathology, inflammatory responses, and ferroptosis-related markers were evaluated. Integrated transcriptomic and metabolomic analyses were performed to identify global regulatory alterations. Mechanistic studies were conducted in erastin-treated HK-2 cells. NRF2 signaling involvement was further assessed using pharmacological inhibition. Results pCA treatment significantly improved renal function, attenuated tubular injury, and suppressed inflammatory responses in FA-induced AKI. Multi-omics integration revealed that pCA markedly reprogrammed metabolic and transcriptional networks associated with ferroptosis and redox homeostasis. Mechanistically, pCA restored antioxidant capacity and normalized the expression of ferroptosis-related proteins. Notably, pCA activated NRF2 signaling, leading to upregulation of downstream targets involved in ferroptosis regulation. Inhibition of NRF2 partially abolished the cytoprotective and anti-ferroptotic effects of pCA in vitro. Conclusion pCA alleviates FA-induced AKI by suppressing ferroptosis through NRF2-dependent regulation of redox and metabolic homeostasis, highlighting NRF2 as a potential therapeutic target for AKI.
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Scientific Reports
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2026
·
IF 4.9
Zhang Panpan,Zhang Xun,Ma Siyu,Jiang Mengqiang,Zhao Wenhong
Astaxanthin (ATX), a natural antioxidant whose benefits in age-related liver and kidney damage remain unclear. We established a D-galactose-induced ageing model in rats and observed the daily behaviour of the rats. Using staining methods to detect ROS, apoptosis and histopathological changes in liver and brain tissue. Determination of antioxidant levels of IL-2, IL-6 and AGES in rats. Assessment of cognitive function using the Morris water maze and ChAT. The mRNA and protein expression levels of Nrf2, Bach1, SOD1, SOD2, HO-1 were determined by real-time PCR and Western blotting. To investigate the role of the Nrf2/Bach1-ARE pathway, we used ML385, a specific inhibitor of the Nrf2 pathway, to treat rats in the inhibitor group. Aging rats showed impaired learning and memory, along with decreased levels of neurotransmitters and antioxidant enzymes. ATX and vitamin E (VE) interventions significantly alleviated these symptoms and activated the Nrf2/Bach1-ARE pathway in liver and brain tissues of aged SD rats. Furthermore, the protective effects of ATX were attenuated by the addition of the Nrf2 inhibitor ML385. ATX reduces oxidative stress and ameliorates liver and brain damage in aged rats via activation of the Nrf2/Bach1-ARE pathway.
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SOUTH AFRICAN JOURNAL OF BOTANY
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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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INTERNATIONAL IMMUNOPHARMACOLOGY
·
2023
·
IF 5.6
Zhehuan Wang,Huiru Zhang,Caihong Qi,Hui Guo,Xiangyue Jiao,Jia Yan,Yifei Wang,Qiangsheng Li,Mingming Zhao,Xinhao Guo,Baoluo Wan,Xiaotian Li
Background Ursolic acid (UA) is a triterpenoid compound found in natural plants. It has been reported to have anti-inflammatory, antioxidant, and immunomodulatory properties. However, its role in atopic dermatitis (AD) is unknown. This study aimed to evaluate the therapeutic effect of UA in AD mice and explore the underlying mechanisms. Methods Balb/c mice were treated with 2, 4-dinitrochlorobenzene (DNCB) to induce AD-like lesions. During modeling and medication administration, dermatitis scores and ear thickness were measured. Subsequently, histopathological changes, levels of T helper cytokines, and oxidative stress markers levels were evaluated. Immunohistochemistry staining was used to assess changes in the expression of the nuclear factor of kappa B (NF-κB) and NF erythroid 2-related factor 2 (Nrf2). Furthermore, CCK8 assay, reactive oxygen species (ROS) assay, real-time PCR, and western blotting were employed to evaluate the effects of UA on ROS levels, inflammatory mediator production, and the NF-κB and Nrf2 pathways in TNF-α/IFN-γ-stimulated HaCaT cells. Results The results showed that UA significantly reduced dermatitis score and ear thickness, effectively inhibited skin proliferation and mast cell infiltration in AD mice, and decreased the expression level of T helper cytokines. Meanwhile, UA improved oxidative stress in AD mice by regulating lipid peroxidation and increasing the activity of antioxidant enzymes. In addition, UA inhibited ROS accumulation and chemokine secretion in TNF-α/IFN-γ-stimulated HaCaT cells. It might exert anti-dermatitis effects by inhibiting the TLR4/NF-κB pathway and activating the Nrf2/HO-1 pathway. Conclusion Taken together, our results suggest that UA may have potential therapeutic effects on AD and could be further studied as a promising drug for AD treatment.
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Toxins
·
2022
·Vol. 14
·期 12
·876
·
IF 5.075
Yanan Wang,Jiayu Wu,Lingfeng Wang,Ping Yang,Zuhong Liu,Shahid Ali Rajput,Mubashar Hassan,Desheng Qi
Aflatoxin B1(AFB1) exists widely in feed and food with severe hazards, posing a serious threat to human and animal health. Epigallocatechin gallate (EGCG) and glutathione (GSH) have been reported as having anti-oxidative and other functions. The present study aimed to investigate the detoxification effect of EGCG and GSH alone or in combination on AFB1exposure in ducklings. Fifty one-day-old male ducklings were randomly assigned into five experimental groups (n= 10): 1. Control (CTR); 2. 0.3 mg/kg BW AFB1(AFB1); 3. 0.3 mg/kg BW AFB1+ 100 mg/kg BW EGCG (AFB1+ EGCG); 4. 0.3 mg/kg BW AFB1+ 30 mg/kg BW GSH (AFB1+ GSH); 5. 0.3 mg/kg BW AFB1+ 100 mg/kg BW EGCG + 30 mg/kg BW GSH (AFB1+ EGCG + GSH). The experiment lasted for seven days. Compared with the CTR group, AFB1reduced growth performance, total serum protein and albumin content, increased serum enzyme activity (alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and γ-glutamyl transpeptidase), and caused pathological damage to the ducklings’ livers. AFB1exposure increased malondialdehyde content and decreased superoxide dismutase, total antioxidant capacity, catalase, glutathione peroxidase activities, and glutathione content in the liver. EGCG and GSH alone or in combination mitigated these adverse effects. Meanwhile, EGCG and GSH attenuate apoptosis of hepatocytes, and regulated AFB1-induced changes in the abundance of genes contained in the Keap1/Nrf2 signalling and apoptotic pathways. Collectively, these results suggest that EGCG and GSH alleviate the hepatocyte injury induced by AFB1by inhibiting oxidative stress and attenuating excessive mitochondria-mediated apoptosis.Keywords:aflatoxin B1;duckling;epigallocatechin gallate;glutathione;oxidative stress;Keap1/Nrf2 signalling;apoptosisKey Contribution:EGCG and GSH alleviate AFB1-induced liver injury in ducklings by increasing antioxidant capacity and antagonising apoptosis.
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PESTICIDE BIOCHEMISTRY AND PHYSIOLOGY
·
2023
·
IF 4.7
Guanglu Wang,Jiajia Guo,Yeyun Ma,Yue Xin,Xiaomeng Ji,Ying Sun,Jian Zhang,Jingquan Dong
The increasing concern over environmental pollution caused by the pesticide avermectin used in aquaculture has attracted significant attention. The use of avermectin, a neurotoxic pesticide, in aquatic environments leads to toxic effects on non-target organisms, particularly causing harm to fish. The phenolic compound ferulic acid possesses excellent anti-inflammatory and antioxidant capabilities. This study was conducted by establishing a chronic exposure experiment to avermectin, proposes the use of ferulic acid as a dietary additive to protect the carp brain from damage caused by exposure to avermectin. Furthermore, it investigates the anti-inflammatory and antioxidant effects of ferulic acid in the carp brain under chronic exposure to avermectin. The experimental results demonstrate that ferulic acid can alleviate brain tissue inflammation and oxidative stress by modulating the Nrf2/Keap1 and NF-κB signaling pathways . It protects the carp brain from chronic avermectin-induced damage, preserves the integrity of the carp blood-brain barrier, enhances the levels of feeding factors, and thereby alleviates carp growth inhibition. These findings provide new therapeutic strategies and a theoretical foundation for the sustainable development of carp aquaculture.
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Journal of Inflammation-London
·
2023
·Vol. 20
·期 1
·1-11
·
IF 5.1
Zhao Ziwen,Xu Zhao,Chang Jingwen,He Liwei,Zhang Zijin,Song Xiaoyu,Hou Xianbang,Fan Fangtian,Jiang Zhijun
Background Ferroptosis in alveolar and bronchial epithelial cells is one of the main mechanisms underlying the development of chronic obstructive pulmonary disease (COPD). Sodium pyruvate (NaPyr) is a natural antioxidant in the body, exhibiting anti-inflammatory and antioxidant activities. NaPyr has been used in a Phase II clinical trial as a novel therapy for COPD; however, the mechanism underlying NaPyr-mediated therapeutic benefits in COPD is not well understood. Objective We aimed to assess the protective effects of NaPyr and elucidate its potential mechanism in cigarette smoke extract (CSE)-induced ferroptosis.To minic the inflammatory response and ferroptosis triggered by cigarette smoke in COPD in an invitro cell based system, we expose a human bronchial epithelial cells to CSE. Methods To minic the inflammatory response and ferroptosis triggered by cigarette smoke in COPD in an invitro cell based system, the A549 (human lung carcinoma epithelial cells) and BEAS-2B (bronchial epithelial cells) cell lines were cultured, followed by treatment with CSE. To measure cellular viability and iron levels, we determined the levels of malondialdehyde (MDA), glutathione (GSH), reactive oxygen species (ROS), mitochondrial superoxide (MitoSOX), membrane potential (MMP), and inflammatory factors (tumor necrosis factor [TNF] and interleukin [IL]-8), and examined CSE-induced pulmonary inflammation and ferroptosis. To clarify the molecular mechanisms of NaPyr in COPD therapy, we performed western blotting and real-time PCR (qPCR) to determine the expression of glutathione peroxidase 4 (GPX4), nuclear factor E2-related factor 2 (Nrf2), and cyclooxygenase 2 (COX2). Results We found that NaPyr effectively mitigated CSE-induced apoptosis and improved apoptosis induced by erastin, a ferroptosis inducer. NaPyr significantly decreased iron and MDA levels and increased GSH levels in CSE-induced cells. Furthermore, NaPyr suppressed ferroptosis characteristics, such as decreased levels of ROS, MitoSOX, and MMP. NaPyr significantly increases the expression levels of GPX4 and Nrf2, indicating that activation of the GPX4/Nrf2 axis could inhibit ferroptosis in alveolar and bronchial epithelial cells. More importantly, NaPyr inhibited the secretion of downstream inflammatory factors, including TNF and IL-8, by decreasing COX2 expression levels to suppress CSE-induced inflammation. Conclusion Accordingly, NaPyr could mitigate CSE-induced ferroptosis in alveolar and bronchial epithelial cells by activating the GPX4/Nrf2 axis and decreasing COX2 expression levels. In addition, NaPyr reduced the secretion of inflammatory factors (TNF and IL-8), affording a novel therapeutic candidate for COPD. Graphical Abstract
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