PHYTOMEDICINE
·
2026
·
IF 11.3
Linyan Lang,Yiping Fu,Jinxin Miao,Yagang Song,Xiaolei Zhang,Quanyou Zhao,Yuting Liu,Yu Zhang,Mingsan Miao,Xingyi Liu,Yueyang Zhang,Xiaoran Wang,Zhanzhan Li
In this study, we report that Fresh Rehmannia glutinosa extract (RGE), effectively prevents and treats Henoch-Schönlein Purpura (HSP) by regulating the PI3K-AKT-mTOR signaling pathway to restore the Treg/Th17 balance. • RGE, a traditional "medicinal and edible homology" herb recently added to China's 2024 list, demonstrates therapeutic potential for HSP by aligning with the TCM principle of "clearing descending fire and nourishing yin" to treat blood syndromes. • RGE and its core active component catalpol significantly alleviate HSP symptoms, reducing skin and renal purpura, pathological damage, and IgA deposition in mouse models. • RGE and its core active component catalpol restore Treg/Th17 balance and suppresses inflammatory cytokines by inhibiting the PI3K-AKT-mTOR/NF-κB signaling pathway, as confirmed by network pharmacology, molecular docking, and in vivo/in vitro experiments. • Multi-omics analysis reveals that RGE intervention reshapes gut microbiota structure and regulates metabolic homeostasis, suggesting a protective "gut-microbiota-immune" mechanism in HSP treatment. Background Therapeutic choices remain limited for Henoch-Schönlein purpura (HSP), an IgA-associated vasculitis. Rehmannia glutinosa , a medicinal and edible herb traditionally used to "clear heat and cool blood," shows clinical promise, yet its precise pathogenesis remains elusive. Purpose This study was designed to examine the therapeutic impact of Rehmannia glutinosa extract (RGE) on HSP, characterize its primary active components, and explore the mechanistic basis of its activity. Study design An integrative approach encompassing in vivo and in vitro HSP models, network pharmacology, LC-MS, molecular docking, dynamics simulations, microbiomics, and metabolomics was utilized to systematically identify the anti-HSP material basis and underlying mechanisms of RGE. Methods Forty-one active components in RGE were identified via LC-MS. A multi-level computational strategy-encompassing network pharmacology, docking studies, and molecular dynamics was applied to screen and identify Catalpol (Cat) as the key active candidate. ICR mouse HSP models and cell cultures were treated with RGE or Cat. Pathological injuries, IgA deposition, and immune cell proportion changes were evaluated using RT-qPCR, Western blot, flow cytometry, and multiplex immunofluorescence. Furthermore, microbiomics and metabolomics were utilized to decipher the mechanism by which RGE exerts its effects through gut microbiota regulation. Results RGE and Cat significantly alleviated skin and kidney injuries and reduced abnormal IgA deposition. By suppressing the PI3K-AKT-mTOR/NF-κB pathway, they successfully rectified the Treg/Th17 imbalance and mitigated inflammatory cytokine production. Additionally, RGE effectively reshaped the gut microbiota ecology and regulated the metabolome. Molecular simulations further confirmed Cat as a key active compound. Conclusion RGE exerts therapeutic effects on HSP through multi-target immunomodulation and gut microbiota remodeling, with Cat identified as a critical active component. These data support the herapeutic prospects of RGE and Cat in the prophylaxis and management of HSP. Download: Download high-res image (351KB) Download: Download full-size image
✓ 已验证
产品关联
DOI
高影响因子
PLoS One
·
2025
·Vol. 20
·期 12
·e0337214
·
IF 2.6
Ruifang Li,Yan Sun,Drolma Kelsang,Mingzhi Feng,Hanhui Cai,Jun Zhang
Background
Ulcerative colitis (UC) is an idiopathic, chronic inflammatory disease of the colon that imposes a significant global public health burden due to its recurrent and refractory nature. The therapeutic effects of butyrate on UC have been documented previously, but its specific mechanisms remain unclear.
Objective
This study aimed to investigate the effects and potential mechanisms of butyrate in dextran sulfate sodium (DSS)-induced UC.
Methods
A UC mouse model was induced utilizing 3% DSS, followed by interventions of 300 mg/kg, 600 mg/kg, or 1200 mg/kg of butyrate. The fecal condition and colonic pathology of the mice were observed, along with measurements of body weight and colon length. The expression of serum inflammatory factors, autophagy-related proteins, and the PI3K/AKT/mTOR pathway-related proteins were detected. Additionally, the impact of butyrate on the mouse gut microbial communities was evaluated using 16S rRNA sequencing technology.
Results
It was demonstrated that butyrate effectively alleviated UC symptoms, including bloody stools, weight loss, and colon shortening. Furthermore, butyrate reduced colonic tissue damage, decreased the expression of TNF-α, IL-1β, and IL-6, and significantly upregulated Beclin-1, Atg5, and the LC3II/I ratio, while reducing P62 expression. Butyrate also decreased the relative expression of p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR. 16S rRNA sequencing results revealed that butyrate improved the intestinal microbial community structure by inhibiting harmful bacteria and accelerating the growth of beneficial bacteria.
Conclusion
This study suggests that butyrate may alleviate DSS-induced UC in mice by blocking the PI3K/AKT/mTOR pathway to facilitating autophagy in intestinal epithelial cells and by modulating the gut microbiota.
研究领域:
免疫学
·
胃肠病学
·
微生物学
·
分子生物学
·
营养科学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
·
2022
·Vol. 395
·期 10
·1283-1295
·
IF 3.195
Xiong Ziwei,Cui Yushun,Wu Jiahui,Shi Lingyu,Quan Wen,Yang Shilin,Feng Yulin
Pteris cretica L. var. nervosa is one of the most well-known Chinese medicines. Although it is widely used to treat jaundice hepatitis, the main ingredient for its treatment was not thoroughly explored until recently. Essentially, the purpose of this study is to find the monomer compound in Pteris cretica L. var. nervosa , which is most likely to be effective in treating liver injury. Through the model of LPS/D-gal-induced liver injury in mice, the best therapeutic site of the total extract was explored, the chemical components of the parts with the best therapeutic effect were separated, a total of 10 flavonoids were isolated, and the RAW264.7 cells induced by LPS were used as the experimental model to explore the preliminary anti-inflammatory activity of NO production in vitro. Finally, the anti-inflammatory activity and the highest content in this plant Luteolin-7-O-rutinoside (LUT) were selected, as the object of study in vivo. It was found that LUT could not only reduce alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, but also significantly reduce the release of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β), and inhibit PI3K/AKT/AMPK/NF-κB pathway. In addition, LUT can increase levels of SOD and GSH to reduce oxidative stress. It has an obvious therapeutic effect on acute liver injury induced by LPS/D-gal in mice. Therefore, infer LUT is a functional substance in Pteris cretica L. var. nervosa. Graphical abstract
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2023
·Vol. 24
·期 20
·15403
·
IF 5.6
Li Chen,Meng Tian,Jing Yang,Zhenxu Wu
Polymer microspheres have recently shown outstanding potential for bone tissue engineering due to their large specific surface area, good porosity, injectable property, good biocompatibility, and biodegradability. Their good load-release function and surface modifiability make them useful as a carrier of drugs or growth factors for the repair of bone defects in irregularly injured or complex microenvironments, such as skull defects. In this study, berberine (BBR)-encapsulated poly(lactic-co-glycolic acid) (PLGA)/hydroxyapatite (HA) microspheres were fabricated using electrified liquid jets and a phase-separation technique, followed by modification with the 3,4-hydroxyphenalyalanine-containing recombinant insulin-like growth–factor-1 (DOPA-IGF-1). Both the BBR and the IGF-1 exhibited sustained release from the IGF-1@PLGA/HA-BBR microspheres, and the composite microspheres exhibited good biocompatibility. The results of the alkaline phosphatase (ALP) activity assays showed that the BBR and IGF-1 in the composite microspheres synergistically promoted the osteogenic differentiation of MC3T3-E1 cells. Furthermore, it was confirmed that immobilized IGF-1 enhances the mRNA expression of an osteogenic-related extracellular matrix and that BBR accelerates the mRNA expression of IGF-1-mediated osteogenic differentiation and cell mineralization. Further cellular studies demonstrate that IGF-1 could further synergistically activate the IGF-1R/PI3K/AKT/mTOR pathway using BBR, thereby enhancing IGF-1-mediated osteogenesis. Rat calvarial defect repair experiments show that IGF-1@PLGA/HA-BBR microspheres can effectively promote the complete bony connection required to cover the defect site and enhance bone defect repair. These findings suggest that IGF-1@PLGA/HA-BBR composite microspheres show a great potential for bone regeneration.Keywords:polymer microspheres;berberine (BBR);IGF-1;bone regeneration;osteogenic differentiation
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
·
2016
·Vol. 38
·期 6
·1871-1878
·
IF 2.348
Xusheng Yuan,Junjun Chen,Min Dai
Paeonol (2'-hydroxy-4'-methoxyacetophenone) is an active component isolated from the root of Paeonia Suffruticosa Andrews. We previously found that paeonol inhibited vascular cell adhesion molecule-1 (VCAM‑1) expression, and thus may be useful for the prevention and treatment of rabbit atherosclerosis (AS); however, the underlying mechanisms are not yet well known. Recently, microRNAs (miRNAs or miRs) have been reported to play an important role in the pathogenesis of AS. In the present study, we examined the effects of paeonol on miRNA-126 (miR‑126) expression, and its ability to inhibit monocyte adhesion to oxidized low-density lipoprotein (ox-LDL)-injured vascular endothelial cells (VECs). VECs were isolated from the rat thoracic aorta and stimulated with ox-LDL (20 mg/l) in the presence of paeonol. We found that miR‑126 had a lower expression in the ox-LDL-injured VECs, and VCAM‑1 was identified as a target gene of miR‑126. Furthermore, paeonol promoted miR‑126 expression and suppressed VCAM‑1 expression at the mRNA and protein level. It also inhibited monocyte adhesion to ox-LDL-injured VECs through the promotion of miR‑126 expression. Furthermore, it was demonstrated that paeonol blocked the activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/nuclear factor-κB (NF-κB) signaling pathway by promoting miR-126 expression. Taken together, and to the best of our knowledge, the findings of this study provide the first evidence that paeonol promotes miR‑126 expression to inhibit monocyte adhesion to ox-LDL-injured VECs and block the activation of the PI3K/Akt/NF-κB signaling pathway. Our data suggest that miR‑126 plays a crucial role in vascular inflammation and may be an important therapeutic target in the treatment of AS with the use of paeonol.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
FOOD RESEARCH INTERNATIONAL
·
2024
·
IF 7
Chengyu Jin,Chu Chu,Xianghai Zhu,Yuanchao Lu,Ningxiang Yu,Qin Ye,Yuanxiang Jin,Xianghe Meng
Camellia oleifera Abel ( C. oleifera ) is a multifunctional oilseed, which is rich in many biological active substances with health-promoting properties, especially polyphenols. Previous research revealed that camellia oil phenolics exhibited anti-inflammatory effect, which originated from seed. Thus, we aimed to explore the components of camellia seed phenolics and its potential mechanism of anti-inflammation. Initially, fractional extraction was processed to prepare the phenolics from camellia seed kernels, and we compare four different fractions of phenolics under the LPS-induced Caco-2/RAW264.7 coculturing model. Results showed that free phenolics (FP) had best effect on alleviating pro-inflammatory cytokines (IL-1β, IL-6, IL-8 and TNF-α) compared to esterified-bound phenolics (EP), glycosylated-bound phenolics (GP) and insoluble-bound phenolics (IP). Furthermore, FP reduced inflammation by suppressing the PI3K/Akt/NF-κB signaling pathway and effectively inhibited LPS-induced intestinal permeability increase, tight junction related proteins loss (ZO-1, claudin-1). Same results obtained, as the transepithelial electrical resistance (TEER) and alkaline phosphatase (AKP) activity of high-dose FP treated group was high than model group. Finally, molecular docking was used for evaluating the anti-inflammatory effect for phenolic monomer. KGRG (kaempferol −3-O-(2-O-glucopyranosyl-6-O-rhamnopyranosyl)-glucopyranoside), KXR (kaempferol 3-O-(2′’-xylopyranosyl)-rutinoside) and leucoside (kaempferol 3-O-sambubioside) show lower binding energy docking with NF-κB, PI3K and Akt protein, indicating better interactions, which might be effective constituents against inflammation. Subsequently, five major polyphenols were obtained to validate the docking results, especially, indicating the best anti-inflammatory activities of KGRG. Overall, this research sheds insights on the therapy of phenolics from C. oleifera seed towards LPS-induced intestinal inflammation model in vitro and its related mechanism.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ACS Applied Materials & Interfaces
·
2025
·
IF 8.2
Shikang Zheng,Xiumei Sun,Kai Chen,Mingjun Zhang,Chentong Zou,Lin Wang,Zhipeng Guo,Zhaoyi Jin,Ziyi Ma,Guanyu Li,Guomin Wu
Critical-sized bone defect regeneration remains a significant clinical challenge due to the complex cascade of biological processes involved. To address this, we developed a sophisticated hierarchical biomembrane (PCS@MPN10) designed to modulate the osteogenic microenvironment. Using coaxial electrospinning, we fabricated a core–shell structure with polylactic acid (PLA) as the membrane base, incorporating simvastatin in the core and chitosan in the shell. The membrane surface was further modified with a tannic acid-iron metal-polyphenol network coating. Our results demonstrated that the biomembrane exhibits excellent biocompatibility, photothermal properties, and significant antibacterial activity. Additionally, the membrane regulates the microenvironment by promoting M1-to-M2 macrophage polarization, showing strong osteogenic potential both in vitro and in vivo. Furthermore, PCS@MPN10+NIR modulates mitochondrial function through the PI3K-AKT pathway, clears mitochondrial reactive oxygen species (ROS), and alleviates cellular oxidative stress, thereby enhancing bone regeneration. Overall, these findings suggest that this biomembrane holds great promise as a strategy for improving bone regeneration in critical-sized defects.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2025
·
IF 5.4
Xiaolong Feng,Xinru Tao,Penghui Li,Jun Chen,Kaiyi Chen,Jinsheng Jiang,Yuan Cai,Yanmei Peng
Ethnopharmacological relevance Yuye Jiedu Granule (YYJD), a traditional herb preparation developed by Hunan Changde Sanjin Pharmaceutical Co., Ltd., has been used in clinical settings for many years to manage upper respiratory tract infections (URTI) attributed to exogenous wind-heat. Although its effectiveness is well recognized, the active constituents responsible for its effects and the molecular pathways involved are not clear yet. Aim of the study To identify the bioactive constituents of YYJD and elucidate its molecular mechanisms in treating URTI. Materials and methods Initially, the chemical composition of YYJD was analyzed using ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS/MS) in combination with a molecular networking approach. Anti-inflammatory components within the formula were then identified using a UPLC-based separation system and a dual-luciferase reporter gene screening assay, followed by in vitro validation. Subsequently, an acute pneumonia model was developed using Pseudomonas aeruginosa infection to comprehensively assess the therapeutic efficacy of YYJD through integrated transcriptomic, metabolomic, and network pharmacology analyses. Finally, the underlying molecular mechanisms were experimentally confirmed. Results A total of 145 chemical constituents were identified in YYJD, among which 15 were found to inhibit NF-κB. In vivo studies demonstrated that YYJD notably decreased mortality, lung indices, and serum pro-inflammatory cytokines in P. aeruginosa -infected mice. Integrated multi-omics analysis highlighted adenosine monophosphate (AMP) as a central metabolite, with major bioactive compounds classified as organic acids, flavonoids, iridoid glycosides, and triterpenoid saponins . Nine pivotal targets and the AMPK-mTORC1/2-PI3K/Akt/NF-κB axis were identified as central to YYJD’s anti-URTI effects. Mechanistically, YYJD modulated the phosphorylation of GSK3β, Akt, IκBα, mTOR, and AMPK, along with the p65 expression. Conclusion This study presents the first in-depth analysis of YYJD’s chemical profile and elucidates its multi-target therapeutic mechanisms against URTI through AMPK-centered metabolic-inflammatory interplay. These results offer a stronger scientific foundation for the clinical use of YYJD and introduce a potential new approach for treating respiratory infections.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Heliyon
·
2023
·
IF 4
Huaxi Liu,Weijie Chen,Chunyang Tian,Yijian Deng,Liangwo Xu,Wenkun Ouyang,Renjie Qiu,Yanting You,Pingping Jiang,Lin Zhou,Jingru Cheng,Hiu Yee Kwan,Xiaoshan Zhao,Xiaomin Sun
Background IgA nephropathy (IgAN) is a major and growing public health problem. Renal fibrosis plays a vital role in the progression of IgAN. This study is to investigate the mechanisms of action underlying the therapeutic effects of Shenbing Decoction II (SBDII) in IgAN renal fibrosis treatment based on ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS), network pharmacology and experimental verification. Method We first used UPLC-MS/MS to explore the main compounds of SBDII, and then used network pharmacology to predict the targets and key pathways of SBDII in the treatment of IgAN renal fibrosis. Next, bovine serum albumin (BSA), lipopolysaccharide (LPS), and carbon tetrachloride (CCL4) were used to induce IgAN in rats, and then biochemical indicators, renal tissue pathology, and renal fibrosis-related indicators were examined. At the same time, part of the results predicted by network pharmacology were also verified. Result A total of 105 compounds were identified in SBDII by UPLC-MS/MS. Network pharmacology results showed that the active compounds such as acacetin, eupatilin, and galangin may mediate the therapeutic effects of SBDII in treating IgAN by targeting tumor protein p53 (TP53) and regulating phosphatidylinositol 3-kinase (PI3K)-Akt kinase (Akt) signaling pathway. Animal experiments showed that SBDII not only significantly improved renal function and fibrosis in IgAN rats, but also significantly downregulated the expressions of p53, p-PI3K and p -Akt. Conclusion This UPLC-MS/MS, network pharmacological and experimental study highlights that the TP53 as a target, and PI3K-Akt signaling pathway are the potential mechanism by which SBDII is involved in IgAN renal fibrosis treatment. Acacetin, eupatilin, and galangin are probable active compounds in SBDII, these results might provide valuable guidance for further studies of IgAN renal fibrosis treatment.
研究领域:
药理学
·
肾病学
·
分子生物学
·
中医药
✓ 已验证
DOI
PubMed
高影响因子
Frontiers in Immunology
·
2024
·
IF 5.7
Long Zhou,Yingxin Yang,Tingjie Li,Yafang Zhao,Jinye Yuan,Chenxin He,Yan Huang,Jinyu Ma,Yue Zhang,Fang Lu,Jiaze Wu,Zijian Li,Hui Kong,Yan Zhao,Huihua Qu
Background: Allergic rhinitis (AR) affects up to 40% of the population, leading to significant healthcare expenditures. Current mainstream treatments, while effective, can lead to side effects and do not address the underlying immunological imbalances. Zingiberis Rhizoma Carbonisatum (ZRC), the partially charred product of Zingiberis Rhizoma (ZR), has been widely used clinically in China since ancient times to treat respiratory disorders.Methods: Inspired by the similarity between high-temperature pyrolysis and carbonization processing of herbal medicine, ZRC derived CDs (ZRC-CDs) were extracted and purified through several procedures. Then, the physicochemical characteristics of CDs were delineated through a suite of characterization methods. Moreover, our investigation zeroed in on elucidating the ameliorative impacts of CDs on ovalbumin-induced rat models alongside their underlying mechanisms.Results: ZRC-CDs with particle sizes ranging from 1.0 to 3.5 nm and rich surface functional groups. Additionally, we observed that ZRC-CDs significantly attenuated nasal symptoms and pathological damage in ovalbumin-induced AR rats, and modulated lipid metabolism and type 2 inflammatory responses. They also inhibit PI3K/AKT and JAK/STAT pathways, which are associated with metabolism and inflammation. Importantly, ZRC-CDs demonstrated high biocompatibility, underscoring their potential as a novel therapeutic agent.Conclusion: ZRC-CDs offer a promising alternative for AR treatment and could help facilitate broader clinical use of the ZRC. In addition, the exploration of the inherent bioactivity of CDs can help to broaden their biological applications.
研究领域:
药理学
·
免疫学
·
纳米技术
·
中医药
✓ 已验证
DOI
高影响因子
NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
·
2026
·
IF 4
Hou Jingyi,Yang Kailan,Zhang Dandan,Ba Yi,Wang Yubo,Zhao Changqi,Zhu Naiqiang,Gu Miao
The increasing global burden of aging-related cognitive impairment (ACI) highlights an urgent need for disease-modifying therapeutics, as current pharmacological options provide only temporary symptomatic relief without affecting underlying pathological trajectories. Ginsenoside Ro, an oleanane-type saponin derived from Panax ginseng, displays anti-inflammatory and cytoprotective properties; however, the target network and signaling mechanisms through which it may alleviate ACI remain inadequately defined. This study aims to thoroughly define the therapeutic efficacy and underlying molecular mechanisms of Ginsenoside Ro against ACI utilizing a convergent analytical approach that integrates network pharmacology, in silico molecular simulation, and empirical validation in aging-model mice and senescent PC12 cells. Putative targets of Ginsenoside Ro were sourced from PubChem, SwissTargetPrediction, STITCH, ChEMBL, and SEA databases. ACI-relevant and aging-associated targets were curated from HAGR, OMIM, and GeneCards databases. A protein–protein interaction (PPI) network was constructed using STRING, and hub targets were identified with the cytoHubba algorithm. Functional enrichment analysis, including GO and KEGG analyses, was performed via DAVID. Binding interactions were evaluated using molecular docking and 100 ns molecular dynamics (MD) simulations. In vivo characterization involved the development of a senescence mouse model via intraperitoneal D-galactose (D-Gal) administration (125 mg/kg/d for 10 weeks), followed by oral treatment with Ginsenoside Ro (5 and 10 mg/kg) or melatonin (100 mg/kg) for 6 weeks. Cognitive performance was assessed using the Morris water maze (MWM) and open field test (OFT). Systemic oxidative status was monitored by measuring serum MDA, SOD, and MAO, while neural tissue integrity was examined through H&E and Nissl staining. In vitro, D-Gal-induced senescent PC12 cells were treated with Ginsenoside Ro (3.125–12.5 µM), followed by evaluations of cell viability, SA- β -galactosidase activity, ROS accumulation, SOD function, and expression levels of TNF-α, IL-6, EGFR, and components of the PI3K-Akt cascade using CCK-8, flow cytometry, RT-qPCR, and Western blot. Target intersection analysis identified 30 overlapping nodes between Ginsenoside Ro and ACI, with TNF-α, IL-6, AKT1, and EGFR recognized as core targets. KEGG enrichment analysis highlighted PI3K-Akt signaling as a key mechanistic pathway. Molecular docking yielded binding energies ranging from − 8.8 to − 4.8 kcal/mol, while MD trajectories demonstrated RMSD/RMSF profiles, hydrogen-bond interactions, and distinct deep free-energy minima consistent with sustained complex formation over the simulation period. In the D-Gal mouse model, Ginsenoside Ro reduced escape latency, increased platform crossings and exploratory behavior, decreased serum MDA, restored SOD and MAO levels, and ameliorated neuronal loss and nuclear pyknosis in the hippocampus and cortex. In PC12 cells, Ginsenoside Ro improved viability, diminished SA- β -gal positivity and ROS accumulation, enhanced SOD activity, restored EGFR expression, suppressed IL-6/TNF-α induction, and normalized the elevated p-PI3K/PI3K and p-AKT/AKT ratios. These findings suggest that Ginsenoside Ro is associated with the modulation of TNF-α, IL-6, AKT1, and EGFR, and that the PI3K-Akt pathway may serve as a central axis correlated with its observed neuroprotective effects. Ginsenoside Ro emerges as a promising candidate for ameliorating aging-associated cognitive dysfunction and related pathological changes, providing a preclinical basis for future translational development.
✓ 已验证
DOI
高影响因子
Journal of Bioresources and Bioproducts
·
2025
·
IF 13
Shuang Qi,Hui Yang,Tian Fang,Tingwei Zhang,Bo Jiang,Sehrish Manan,Chaofeng Zhang,Peng Wang,Caoxing Huang,Wenjuan Wu,Yongcan Jin
Lignin, a natural and renewable aromatic biopolymer, has gained attention in various biomedical applications due to its diverse structure, excellent biocompatibility, and antioxidant activity. However, the effects of lignin with tailored molecular weight on treating type 2 diabetes mellitus (T2DM) remain largely unexplored. In this study, a series of heterogeneous natural phenolic kraft lignin (KL) with tailored molecular weights, derived through an anti-sugar strategy, were prepared by continuous fractionation. The lignin fractions were categorized as F1, F2, and F3, corresponding to high, medium, and low molecular weights, respectively. Their therapeutic effects on T2DM were evaluated using a fractionated lignin culture cell model and intravenous injection into the tail vein of diabetic rats. The results demonstrated that lignin's protective effects in attenuating T2DM progression were molecular weight-dependent. Specifically, F3 reduced fasting blood glucose, reversed insulin resistance, and improved insulin sensitivity by mitigating oxidative stress and inflammatory responses. Mechanistic investigations revealed that F3 positively regulated glucose and lipid metabolism, inhibited hepatic gluconeogenesis, and enhanced hepatic glycogen synthesis by activating the insulin receptor substrate 1/phosphoinositide 3-kinase/protein kinase B (IRS1/PI3K/AKT) signaling pathway. Results revealed that lignin exerts its therapeutic effects on T2DM in a molecular weight-dependent manner, with IRS1/PI3K/AKT signaling as a potential underlying mechanism. This highlights lignin with a defined molecular weight as a promising candidate for T2DM treatment.
✓ 已验证
产品关联
DOI
高影响因子
危险品化学品经营许可证（带存储）