MICROCHEMICAL JOURNAL
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2026
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IF 5.2
He Bu,Qingling Zhao,Jie Gao,Zixuan Zhang,Ze Liu,Lanlan Li,Xiaofei Yu,Xiaojing Yang,Zunming Lu,Shuquan Zhang,Xinghua Zhang
Fluorescent carbon dots (CDs) derived from traditional Chinese medicine (TCM) face limitations in water solubility and tunable emission, hindering their biomedical application. To address this, we synthesized baicalin-based CDs and engineered their surface with cetyltrimethylammonium chloride (CTAC) and Cu ions. This sequential modification first shifted the emission from blue to orange by introducing N/O-containing functional groups that reduced the energy gap. Subsequent Cu incorporation created Cu-related energy levels, further narrowing the gap to achieve red emission at 660 nm alongside enhanced solubility. In addition, the resulting Cu/CTAC-CDs served as a selective fluorescent probe for histidine, enabling its sensitive detection in complex matrices such as pig blood and milk. This work provides a viable route to fabricate water-soluble, emission-tunable TCM-derived CDs and offers fundamental insights into surface-state-controlled luminescence, advancing their development for biomedical applications.
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Small
·
2026
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IF 11.8
Xi Jiang,Fengqi Yang,Huiling Gong,Yanfei Mou,Junyi An,Lei Wang,Xiaona Wang,Zhenzhen Zhang,Xiao Wei,Li Sun,Wenli Wang,Fenglei Cao,Yang Zhao,Ding Qu
Wet age-related macular degeneration (wAMD), characterized by choroidal neovascularization (CNV), faces a clinical challenge of diminishing efficacy during long-term anti-VEGF monotherapy. An AI-assisted analytical framework pinpointed impaired retinal pigment epithelium (RPE) autophagy and a pro-inflammatory microenvironment driven by retinal microglia-recruited monocytes as co-conspirators in CNV progression. To tackle these dual culprits, we developed an intravitreal injectable hydrogel (Rab&BCL-M@G) that co-encapsulates ranibizumab (Rab) and a small-sized baicalin-loaded microemulsion (BCL-M), enabling controlled and sustained co-delivery of both agents to the retina for over 14 days. Guided by the AI-identified targets, we demonstrated that baicalin promoted dysfunctional mitochondria clearance via the AKT2-PGC-1α-mediated autophagic flux and suppressed monocyte recruitment by disrupting microglial CCL4 signaling. This two-pronged action ameliorated inflammation and angiogenesis, synergizing with Rab. In a laser-induced wAMD mouse model, a single intravitreal injection of Rab&BCL-M@G sustainably reduced CNV area, promoted repair, restored autophagy, and diminished microglial infiltration. Crucially, subsequent wet-lab validation confirmed a positive pathological correlation among defective autophagy, inflammation, and angiogenesis, thereby closing the loop from computational prediction to experimental verification and explaining suboptimal long-term performance after Rab monotherapy. This study proposes a promising synergistic strategy, advancing wAMD therapy through precision delivery and AI-informed mechanism discovery.
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BMC Complementary Medicine and Therapies
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2024
·Vol. 24
·期 1
·1-13
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IF 3.3
Li Jiao,Zhang Qi-Yun,Lu Qing-Yu,Liu Qiao-Zhou,Guo Li,Li Min,Sun Qian-Yun
IntroductionAcute lung injury (ALI) as one kind of acute pulmonary inflammatory disorder, manifests primarily as damage to alveolar epithelial cells and microvascular endothelial cells. Activation of the complement system is a common pathological mechanism in ALI induced by diverse factors, with the complement alternative pathway assuming a pivotal role. Baicalin, a flavonoid derived from the root of Scutellaria baicalensis Georgi, exhibits noteworthy biological activities. The present study attempted the interventional effects and underlying mechanisms of baicalin in microangiopathy in ALI induced by complement alternative pathway activation.Methods Activation of the complement alternative pathway by cobra venom factor (CVF). HMEC cells were pretreated with baicalin and then exposed to complement activation products. The expression of inflammatory mediators was detected by ELISA, and the intranuclear transcriptional activity of NF-κB was assessed by a dual fluorescent kinase reporter gene assay kit. Before establishing the ALI mouse model, baicalin or PDTC was gavaged for 7 d. CVF was injected into the tail vein to establish the ALI model. The levels of inflammatory mediators in BALF and serum were determined by ELISA. HE staining and immunohistochemistry evaluated pathological changes, complement activation product deposition, and NF-κB p65 phosphorylation in lung tissue.Results Baicalin reduced complement alternative activation product-induced expression of HMEC cells adhesion molecules (ICAM-1, VCAM-1, E-selectin) and cytokines (IL-6, TNF-α) as well as upregulation of NF-κB intranuclear transcriptional activity. Baicalin intervention reduced the number of inflammatory cells and protein content in the BALF and decreased the levels of IL-6, TNF-α, and ICAM-1 in serum and IL-6, TNF-α, ICAM-1, and P-selectin in BLAF. In addition, baicalin attenuated inflammatory cell infiltration in the lung of ALI mice and reduced the deposition of complement activation products (C5a, C5b-9) and phosphorylation of NF-κB p65 in lung tissue.Conclusion Baicalin relieves complement alternative pathway activation-induced lung inflammation by inhibition of NF-κB pathway, delaying the progression of ALI.
研究领域:
药理学
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免疫学
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肺医学
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PubMed
高影响因子
Scientific Reports
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2025
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IF 3.9
Xu Qiuling,Liu Zhuoxi,Wang Liyuan,Liu Guoyang,Zhao Long,Yue Hui,Liu Yong
Diabetic cardiomyopathy (DCM) requires a systematic approach for effective management. Focusing on key signaling pathways in myocardial fibrosis could offer novel therapeutic approaches for DCM. The objective of this research is to investigate new biomarker and the underlying mechanisms by which baicalin intervenes in the progression of DCM. Swiss Target Prediction databases and weighted correlation network analysis (WGCNA) were employed to collect and analyze targets of baicalin and DCM. Intersection targets were obtained through venn online website, network visualization was conducted through STRING database and Cytoscape 3.7.2 software. Molecular docking validation was completed via AutoDock Vina software. Western blotting, RT-qPCR and histology were carried out to validate the direct targets of baicalin and explore the molecular mechanism during DCM progression. In mice induced to DCM, we observed that disruptor of telomeric silencing 1-like (DOT1L) was upregulated. Baicalin (BC) reduced myocardial fibrosis in mice as indicated by the reduced expression levels of fibrosis markers COL-1 and TGF-β. The inhibitory effect of BC was reversed by overexpressed DOT1L and further enhanced by silenced DOT1L. Our results indicate that cardiomyocyte DOT1L exerts a pathogenic role in DCM and BC specifically targets DOT1L/COL-1 signaling to reduce myocardial fibrosis in DCM.
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Hepatobiliary & Pancreatic Diseases International
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2025
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IF 4.4
Han-Ying Zhou,Ting Li,Yuan-Qiang Lu
Background Diquat, a commonly employed bipyridyl herbicide, is recognized for its hepatotoxic effects attributed to the generation of reactive oxygen species. Baicalin (BAI), a flavonoid derivative, has garnered significant research interest for its hepatoprotective properties. Nevertheless, the clinical application of BAI is constrained by its limited water solubility and poor bioavailability. To address these challenges, BAI-nanoliposome (BAI-NL) has emerged as a novel drug delivery platform aimed at enhancing therapeutic outcomes. Methods We used diquat-induced liver injury mouse model and AML12 hepatocytes to test the protective effect of BAI and BAI-NL on liver inflammation, oxidative stress, and mitochondrial function. The parameters included histological, biochemical, and molecular biological analyses. Results In the diquat-induced model, both BAI and BAI-NL exhibited effectiveness on attenuating liver inflammation. Ex vivo analyses further indicated that BAI-NL was superior to BAI in preserving mitochondrial membrane potential, reducing oxidative stress, and modulating the phosphatase and tensin homolog-induced putative kinase 1 (PINK1)/Parkin RBR E3 ubiquitin-protein ligase (Parkin) signaling pathway. These findings enhanced mitophagy and facilitated the removal of damaged mitochondria. Conclusions BAI-NL exhibited superior hepatoprotective effects compared to free BAI, possibly by reducing inflammation, preserving mitochondrial homeostasis, and reinstating autophagic balance through modulation of the PINK1/Parkin signaling pathway. These outcomes indicate a groundbreaking method for addressing liver diseases and underscore the potential of nanoliposome technology in augmenting the efficacy of natural compounds.
研究领域:
药理学
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毒理学
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生物化学
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分子生物学
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PubMed
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ACTA PHARMACOLOGICA SINICA
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2024
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IF 6.9
You Yi-ping,Yan Liang,Ke Hua-yu,Li Ya-ping,Shi Zi-jian,Zhou Zhi-ya,Yang Hai-yan,Yuan Tao,Gan Ying-qing,Lu Na,Xu Li-hui,Hu Bo,Ou-Yang Dong-yun,Zha Qing-bing,He Xian-hui
PANoptosis is an emerging form of regulated cell death (RCD) characterized by simultaneous activation of pyroptotic, apoptotic, and necroptotic signaling that not only participates in pathologies of inflammatory diseases but also has a critical role against pathogenic infections. Targeting PANoptosis represents a promising therapeutic strategy for related inflammatory diseases, but identification of inhibitors for PANoptosis remains an unmet demand. Baicalin (黄芩苷) is an active flavonoid isolated from Scutellaria baicalensis Georgi (Huangqin), a traditional Chinese medicinal herb used for heat-clearing and detoxifying. Numerous studies suggest that baicalin possesses inhibitory activities on various forms of RCD including apoptosis/secondary necrosis, pyroptosis, and necroptosis, thereby mitigating inflammatory responses. In this study we investigated the effects of baicalin on PANoptosis in macrophage cellular models. Primary macrophages (BMDMs) or J774A.1 macrophage cells were treated with 5Z-7-oxozeaenol (OXO, an inhibitor for TAK1) in combination with TNF-α or LPS. We showed that OXO plus TNF-α or LPS induced robust lytic cell death, which was dose-dependently inhibited by baicalin (50−200 μM). We demonstrated that PANoptosis induction was accompanied by overt mitochondrial injury, mitochondrial DNA (mtDNA) release and Z-DNA formation. Z-DNA was formed from cytosolic oxidized mtDNA. Both oxidized mtDNA and mitochondrial Z-DNA puncta were co-localized with the PANoptosome (including ZBP1, RIPK3, ASC, and caspase-8), a platform for mediating PANoptosis. Intriguingly, baicalin not only prevented mitochondrial injury but also blocked mtDNA release, Z-DNA formation and PANoptosome assembly. Knockdown of ZBP1 markedly decreased PANoptotic cell death. In a mouse model of hemophagocytic lymphohistiocytosis (HLH), administration of baicalin (200 mg/kg, i.g., for 4 times) significantly mitigated lung and liver injury and reduced levels of serum TNF-α and IFN-γ, concomitant with decreased levels of PANoptosis hallmarks in these organs. Baicalin also abrogated the hallmarks of PANoptosis in liver-resident macrophages (Kupffer cells) in HLH mice. Collectively, our results demonstrate that baicalin inhibits PANoptosis in macrophages by blocking mitochondrial Z-DNA formation and ZBP1-PANoptosome assembly, thus conferring protection against inflammatory diseases. PANoptosis is a form of regulated cell death displaying simultaneous activation of pyroptotic, apoptotic, and necroptotic signaling. This study shows that induction of PANoptosis is linked to mitochondrial dysfunction and mitochondrial Z-DNA formation. Baicalin inhibits PANoptosis in macrophages in vitro via blocking mitochondrial dysfunction and the mitochondrial Z-DNA formation and thereby impeding the assembly of ZBP1-associated PANoptosome. In a mouse model of hemophagocytic lymphohistiocytosis (HLH), baicalin inhibits the activation of PANoptotic signaling in liver-resident macrophages (Kupffer cells) in vivo, thus mitigating systemic inflammation and multiple organ injury in mice.
研究领域:
免疫学
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细胞生物学
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药理学
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炎症
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调控性细胞死亡
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INTERNATIONAL IMMUNOPHARMACOLOGY
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2025
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IF 4.7
Yi-fan Li,Yue-fan Zhang,Can Huang,Jie-mei Jiang
Objective The inflammatory response is integral to all stages of ischemic stroke. Unlike conventional reperfusion therapies, anti-inflammatory strategies offer a broader therapeutic window for treating ischemic stroke due to their capacity to attenuate inflammation. Astrocytes, once activated in ischemic conditions, significantly contribute to the production of inflammatory cytokines and exacerbate brain damage. While the neuroprotective effects of baicalin in post-stroke patients have been recognized, its role in modulating astrocyte activity and reducing inflammation remains under debate. This study aims to evaluate the impact of baicalin on astrocyte activation following ischemic stroke. Methods A model of ischemia/reperfusion (I/R) injury was induced in wild-type mice through transient middle cerebral artery occlusion (tMCAO). Mice were randomized into groups receiving either baicalin or saline. The expression levels of inflammatory markers—interleukin (IL)-6, IL-1β, monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-alpha (TNF-α)—were quantified using enzyme-linked immunosorbent assay (ELISA). Additionally, western blot analysis was employed to assess glial fibrillary acidic protein (GFAP) expression. Results Baicalin administration significantly mitigated neurological deficits in mice post-tMCAO. It reduced the activation of astrocytes and the production of pro-inflammatory cytokines such as IL-6, IL-1β, TNF-α, and MCP-1, observed both in vivo and in vitro. In vitro studies also indicated a suppression of NF-κB activation. Conclusion Baicalin effectively prevents ischemic brain damage by curtailing neuroinflammation and astrocyte activation. These findings advance the understanding of baicalin’s mechanistic role in mitigating brain ischemia and support further investigation into its therapeutic potential.
研究领域:
神经科学
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药理学
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EUROPEAN JOURNAL OF PHARMACOLOGY
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2024
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IF 4.2
Yuan Liu,Xiaohui Jin,Caiyin Li,Jingjing Bu,Baoying Wang,Ming Bai,Pan Su,Erping Xu,Yucheng Li
Defective mitophagy is closely related to the neuronal dysfunction and major depressive disorder (MDD). Our previous study found that baicalin could enhance nip-like protein (NIX)-mediated mitophagy and exhibit antidepressant effects, and predicted that AMPK may be the pharmacological target of baicalin. However, validated experiments are lacking. In the present study, we first demonstrated the effect of baicalin on hippocampal NIX-mediated mitophagy in CORT-induced depressive mice. Secondly, we transfected siRNA to knockdown AMPK, PGC-1α, and NIX respectively in HT22 cells, and detected the effects of baicalin on mitochondrial function, AMPK/PGC-1α/NIX pathway protein expression and mitophagy levels. Finally, AAV-shAMPKα was injected into hippocampal CA3 to knockdown AMPK in mice to validate the antidepressant effects of baicalin in vivo. The results showed that CORT induced depressive-like behaviors, accompanied with neuronal damage, mitochondrial injury, and inhibited mitophagy in the hippocampus, which were prevented by baicalin (20 mg/kg) treatment. In HT22 cells, baicalin remarkably ameliorated mitochondrial dysfunction and mitophagy disturbance induced by CORT, and these protective effects of baicalin were blocked by knockdown of AMPK, PGC-1α and NIX. Moreover, the beneficial effects of baicalin on depressive-like behaviors and NIX-mediated mitophagy were suppressed by knockdown of AMPKα in mice. Our present results further demonstrated that baicalin promotes NIX-mediated mitophagy and improves depression in an AMPK-dependent manner.
研究领域:
神经科学
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药理学
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分子生物学
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抑郁症
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FEBS Open Bio
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2024
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IF 2.8
Xin Meng,Mengna Kang,Zhiyun Yu,Changyou Li,Yang Chen,Taicheng Jin,Kai Wang,Haiyong Guo
Methicillin-resistant Staphylococcus aureus (MRSA) poses a challenge for clinical treatment and combining antibiotics with other agents might be a promising strategy to overcome this challenge. This study explored the synergistic antibacterial activity of baicalin (traditional Chinese medicine extract) and the narrow-spectrum beta-lactam antibiotic oxacillin sodium, both of which are poorly active against MRSA in vitro . The combination of baicalin and oxacillin sodium showed a synergistic effect with a fractional inhibitory concentration index of 0.5. Mechanistically, the supplementation of baicalin increased the permeability of bacterial cell walls and cell membranes, enhancing oxacillin sodium entry and bactericidal action. The combination of baicalin and oxacillin sodium also significantly inhibited MRSA USA300 biofilm formation by further reducing polysaccharide intercellular adhesion production. Therefore, the combination of baicalin and oxacillin sodium offers a new therapeutic option for addressing clinical MRSA resistance. Further studies, including clinical trials, will be required to validate the observed in vitro results.
研究领域:
药理学
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微生物学
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传染病学
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Bioactive Materials
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2021
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IF 14.593
Shue Jin,Jing Gao,Renli Yang,Chen Yuan,Ruili Wang,Qin Zou,Yi Zuo,Meifang Zhu,Yubao Li,Yi Man,Jidong Li
We demonstrate a simple, effective and feasible method to address the shrinkage of Poly (lactic- co -glycolic acid) (PLGA) through a core-shell structure fiber strategy. The results revealed that introducing size-stable poly-caprolactone (PCL) as the core fiber significantly improved the PLGA-based fibrous scaffold's dimensional maintenance. We further utilized fish collagen to modify the PLGA shell layer (PFC) of coaxial fibers and loaded baicalin (BA) into the PCL core layer (PCL-BA) to endow fibrous scaffold with more functional biological cues. The PFC/PCL-BA fibrous scaffold promoted the osteogenic differentiation of bone mesenchymal stem cells and stimulated the RAW264.7 cells to polarize into a pro-reparative phenotype. Importantly, the in vivo study demonstrated that the PFC/PCL-BA scaffold could regulate inflammation and osteoclast differentiation, favor neovascularization and bone formation. This work tactfully combined PLGA and PCL to establish a drug release platform based on the core-shell fibrous scaffold for vascularized bone regeneration.
研究领域:
生物医学工程
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组织工程
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再生医学
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药剂学
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JOURNAL OF SEPARATION SCIENCE
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2026
·Vol. 49
·期 4
·e70420
·
IF 3.6
Wen-Zhi Chen,Hao-Nan Chen,Zheng Zhang
This work addresses the challenge of imparting molecular selectivity to metal-organic frameworks (MOFs) by developing a molecularly imprinted polymer based on ZIF-90 (MI-ZIF). Starch was used as a green and multifunctional auxiliary polymer during a room-temperature preparation of MI-ZIF with baicalin as the template. This strategy leverages the hydroxyl groups of starch to orchestrate the formation of specific recognition cavities within the ZIF-90 framework. The well prepared MI-ZIF exhibited high adsorption capacity and good specificity, with an imprinting factor (IF) of 4.1. The MI-ZIF was used to enrich baicalin from complex matrices such as plant extracts and serum samples. It achieved a high adsorption rate of 93.2% for baicalin from a Scutellaria baicalensis Georgi (SBG) root extract, increasing the baicalin purity from 19.7% to 71.3%. As a solid-phase extraction sorbent for the analysis of serum samples, this method showed high sensitivity with a detection limit of 0.9 ng mL −1 and recoveries in the range of 78.2%–97.2%. The results indicate that the MI-ZIF can significantly improve the enrichment efficiency and detection sensitivity of baicalin, providing an efficient and reliable technical means to solve the problems of enrichment, separation, and trace detection of flavonoid compounds in complex samples.
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INTERNATIONAL JOURNAL OF PHARMACEUTICS
·
2026
·
IF 6
Sha Xiong,Wenyao Ying,Ting Xiao,Ziyi Liu,Han Fu,Guihong Chai,Yuehong Xu
Androgenetic alopecia (AGA) is the most prevalent hair loss with conventional drug treatments necessitating prolonged compliance. However, current treatments are limited by side effects, frequent dosing, and the stratum corneum (SC) barrier with topical administration. Baicalin (BA) is a natural ingredient showing promise in treating AGA, but its poor water solubility and low bioavailability limit its clinical application. To address the challenges of BA solubility, skin barrier, and patient compliance, we combined BA nanocrystals (BA-NCs) with dissolving microneedles (MNs) to develop a drug delivery system, BA-NCs@MNs, for effective and long-acting treatment of AGA. The BA-NCs notably increased BA solubility by approximately 30-fold, facilitated cellular uptake, and reversed the abnormal mRNA expressions in dihydrotestosterone-induced hair follicle-associated cells. Furthermore, BA-NCs@MNs effectively overcame the SC barrier, improving BA penetration and skin retention by 6.93- and 11.6-fold, respectively, and most importantly, facilitated preferential delivery and accumulation at hair follicle sites. In an AGA mouse model, BA-NCs@MNs with only one dose every three days showed comparable therapeutic efficacy to commercial minoxidil (5 % w/v) with daily dose. This system mechanistically promoted hair follicle regeneration through remodeling the microenvironment by reducing 5α-reductase and androgen level, upregulating the expression of β-catenin, promoting pericapillary angiogenesis, elevating hair follicle stem cell markers, and relieving oxidative stress. Taken together, BA-NCs@MNs is a synergistic and long-acting approach for treating AGA.
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