BRITISH JOURNAL OF PHARMACOLOGY
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2025
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IF 7.7
Hui Ma,Yue Chen,Yi-Mo Zhang,Yue Zhang,Xiao-Juan Hou,Hai-Long Li,Yi-Xin Yang,Qian Long,Xin Qiao,Yun-Feng Li
Background and Purpose Ischaemic stroke is one of the most critical causes of death and disability worldwide, but its pharmacotherapies are currently lacking. This study aimed to investigate the effects of the sigma non-opioid intracellular receptor 1 agonist hypidone hydrochloride (YL-0919) on ischaemic stroke as well as the underlying mechanisms. Experimental Approach Male mice were subjected to a middle cerebral artery occlusion (MCAO)/reperfusion (R) model to mimic ischaemic stroke injury. Neurological and cognitive functions were evaluated, and neuroinflammatory pathways in the medial prefrontal cortex and hippocampus were detected. Key Results Mice subjected to MCAO exhibited obvious neurological and motor deficits, increased infarct volume and neuronal death in the acute phase, and severe cognitive impairment in the chronic phase. Administration of YL-0919 for seven consecutive days beginning within 7 h after MCAO significantly ameliorated the pathological changes described above. Further studies demonstrated that YL-0919 exerted its effect by suppressing absent in melanoma 2 (AIM2)-related inflammatory signals in MCAO mice and alleviated the neuronal deficits in the medial prefrontal cortex and hippocampus, thereby ameliorating chronic post-stroke cognitive impairment. This effect was eliminated by AIM2 overexpression in the medial prefrontal cortex and hippocampus. Conclusions and Implications This study highlights the extended therapeutic window for sigma non-opioid intracellular receptor 1 agonist administration during the acute phase of ischaemic stroke and further demonstrates that targeted inhibition of AIM2-mediated neuroinflammatory pathways may promote sustained cognitive rehabilitation in post-stroke survivors. Graphical
研究领域:
神经药理学
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卒中研究
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炎症生物学
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认知神经科学
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药物研发
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DOI
PubMed
高影响因子
BRITISH JOURNAL OF PHARMACOLOGY
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2015
·Vol. 172
·期 16
·4052-4065
·
IF 4.842
Lin Guo,Yanke Chen,Rui Zhao,Guanghui Wang,Eitan Friedman,Ao Zhang,Xuechu Zhen
Background and Purpose Application of orthosteric sigma-1 receptor agonists as anti-seizure drugs has been hindered by questionable efficacy and potential adverse effects. Here, we have investigated the anti-seizure effects of the novel and potent allosteric modulator of sigma-1 receptors, SKF83959 and its derivative SOMCL-668 (3-methyl-phenyl-2,3,4,5-tetrahydro-1H-benzo[d]azepin-7-ol). Experimental Approach The anti-seizure effects of SKF83959 were investigated in three mouse models, maximal electroshock seizures, pentylenetetrazole-induced convulsions and kainic acid-induced ‘status epilepticus’. Also, in rats, the cortical epileptiform activity induced by topical application of picrotoxin was recorded in electrocorticograms. In rat hippocampal brain slices, effects of the drugs on the high potassium-evoked epileptiform local field potentials were studied. Anti-seizure activities of SOMCL-668, a newly developed sigma-1 receptor selective allosteric modulator, were also investigated. Key Results SKF83959 (20, 40 mg·kg −1 ) exhibited anti –seizure actitity in the three mouse models and reduced the cortical epileptiform activity without alteration of spontaneous motor activity and motor coordination. These effects were blocked by the sigma-1 receptor antagonist BD1047, but not the dopamine D 1 receptor antagonist SCH23390. SKF83959 alone did not directly inhibit the epileptiform firing of CA3 neurons induced by high potassium in hippocampal slices, but did potentiate inhibition by the orthosteric sigma-1 receptor agonist SKF10047. Lastly, a selective sigma-1 receptor allosteric modulator SOMCL-668, which does not bind to dopamine receptors, exerted similar anti-seizure activities. Conclusions and Implications SKF83959 and SOMCL-668 displayed anti-seizure activities, indicating that allosteric modulation of sigma-1 receptors may provide a novel approach for discovering new anti-seizure drugs.
研究领域:
药理学
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神经科学
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分子生物学
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DOI
PubMed
高影响因子
BRITISH JOURNAL OF PHARMACOLOGY
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2025
·
IF 7.7
Yu-Chen Jiang,Jia Guo,Sai-Hu Liu,Xu Dai,Chen-Yu Wang,Li-Hua Lian,Zhen-Yu Cui,Ji-Xing Nan,Yan-Ling Wu
Background and Purpose Vincamine has extensive biological and pharmaceutical activity. We examined the hepatoprotective effects and mechanisms by which vincamine suppresses hepatic fibrosis. Experimental Approach Hepatic stellate cells (HSCs), TGF- β stimulated, were cultured with either vincamine, farnesoid X receptor (NR1H4; FXR) agonist or antagonist. Further, C57BL/6 mice were given thioacetamide (TAA) to induce hepatic fibrosis and subsequently treated with vincamine or curcumin. Key Results Vincamine regulated the deposition of extracellular matrix (ECM), inflammatory factors and S100A4, and up-regulated FXR and TGR5 (GPBA receptor) in activated HSCs, by activating FXR. FXR deficiency blocked vincamine effect on FXR, TGR5, α -smooth muscle actin ( α -SMA) and IL1R1 in activated LX-2 cells. Vincamine corrected ECM imbalance, inflammatory secretion and FXR/TGR5 down-regulation in activated LX-2 cells with stimulating medium from LPS-primed THP-1 cells. S100A4 deficiency increased FXR and TGR5, and decreased IL-1β expression in activated THP-1. Further, S100A4 deficiency in activated macrophages could elevate FXR and TGR5 expression in activated LX-2, strengthening the impact of vincamine on α -SMA and IL-1β expression. Further, vincamine reduced serum ALT/AST levels, liver and intestinal histopathological changes, and caused ECM accumulation and protected the intestinal barrier in thioacetamide-induced hepatic fibrosis mice. Vincamine decreased inflammatory factors e.g. caspase 1 and IL-1β, and inhibited the S100A4-mediated FXR-TGR5 pathway. Conclusion and Implications Vincamine significantly reverses hepatic fibrosis via inhibiting S100A4 involved in the crosstalk between macrophages and HSCs, and by activating the FXR-TGR5 pathway. Targeting the S100A4-mediated FXR dependence on modulating the liver environment may be the key target of vincamine in inhibiting hepatic fibrosis. Graphical
研究领域:
药理学
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肝脏病学
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分子生物学
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DOI
PubMed
高影响因子
BRITISH JOURNAL OF PHARMACOLOGY
·
2024
·
IF 6.8
Yunfu Shen,You Yang,Zi Wang,Wanjun Lin,Na Feng,Meina Shi,Jiachen Liu,Wenzhe Ma
Background and Purpose Triple-negative breast cancer (TNBC) has a poor prognosis due to limited therapeutic options. Recent studies have shown that TNBC is highly dependent on mitochondrial oxidative phosphorylation. The aim of this study was to investigate the potential of coptisine, a novel compound that inhibits the complex I of the mitochondrial electron transport chain (ETC), as a treatment for TNBC. Experimental Approach In this study, mitochondrial metabolism in TNBC was analysed by bioinformatics. In vitro and in vivo experiments (in mice) were conducted to evaluate the potential of coptisine as an ETC complex I-targeting therapeutic agent and to investigate the molecular mechanisms underlying coptisine-induced mitochondrial dysfunction. The therapeutic effect of coptisine was assessed in TNBC cells and xenograft mouse model. Key Results We demonstrated that mitochondrial ETC I was responsible for this metabolic vulnerability in TNBC. Furthermore, a naturally occurring compound, coptisine, exhibited specific inhibitory activity against this complex I. Treatment with coptisine significantly inhibited mitochondrial functions, reprogrammed cellular metabolism, induced apoptosis and ultimately inhibited the proliferation of TNBC cells. Additionally, coptisine administration induced prominent growth inhibition that was dependent on the presence of a functional complex I in xenograft mouse models. Conclusion and Implications Altogether, these findings suggest the promising potential of coptisine as a potent ETC complex I inhibitor to target the metabolic vulnerability of TNBC. Graphical
研究领域:
肿瘤学
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分子生物学
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药理学
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DOI
PubMed
高影响因子
BRITISH JOURNAL OF PHARMACOLOGY
·
2024
·
IF 6.8
Siyue Chen,Yuming Liu,Yutian Zhang,Xu Guo,Tinghui Bai,Kai He,Yanfang Zhu,Yi Lei,Mei Du,Xiaohong Wang,Qiang Liu,Hua Yan
Background and Purpose Pathological retinal angiogenesis is a typical manifestation of vision-threatening ocular diseases. Many patients exhibit poor response or resistance to anti-vascular endothelial growth factor (VEGF) agents. Bruton's tyrosine kinase (BTK) controls the proliferation and function of immune cells. Therefore, we examined the anti-inflammatory and anti-angiogenic effects of BTK inhibition on retinal angiogenesis. Experimental Approach Retinal neovascularisation and vascular leakage in oxygen-induced retinopathy in C57/BL6J mice were assessed by whole-mount retinal immunofluorescence. PLX5622 was used to deplete microglia and Rag1 -knockout mice were used to test the contribution of lymphocytes to the effects of BTK inhibition. The cytokines, activation markers, inflammatory and immune-regulatory activities of retinal microglia/macrophages were detected using qRT-PCR and immunofluorescence. NLRP3 was detected by western blotting, and the effects of BTK inhibition on the co-culture of microglia and human retinal microvascular endothelial cells (HRMECs) were examined. Key Results BTK inhibition suppressed pathological angiogenesis and vascular leakage, and significantly reduced retinal inflammation, which involved microglia/macrophages but not lymphocytes. BTK inhibition increased anti-inflammatory factors and reduced pro-inflammatory cytokines that resulted from NLRP3 inflammasome activation. BTK inhibition suppressed the inflammatory activity of microglia/macrophages, and acted synergistically with anti-VEGF without retinal toxicity. Moreover, the supernatant of microglia incubated with BTK-inhibitor reduced the proliferation, tube formation and sprouting of HRMECs. Conclusion and Implications BTK inhibition suppressed retinal neovascularisation and vascular leakage by modulating the inflammatory activity of microglia and macrophages. Our study suggests BTK inhibition as a novel and promising approach for alleviating pathological retinal angiogenesis. Graphical
研究领域:
眼科学
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免疫学
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药理学
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分子生物学
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DOI
PubMed
高影响因子
BRITISH JOURNAL OF PHARMACOLOGY
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2024
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IF 6.8
Chang Di,Tong Wu,Kai Gao,Na Li,Huifang Song,Lili Wang,Haojie Sun,Jingyun Yi,Xinran Zhang,Jiexin Chen,Mala Shah,Yuwu Jiang,Zhuo Huang
Background and Purpose KCNT1 encodes a sodium-activated potassium channel (Slack channel), and its mutation can cause several forms of epilepsy. Traditional antiepileptic medications have limited efficacy in treating patients with KCNT1 mutations. Here, we describe one heterozygous KCNT1 mutation, M267T, in a patient with EIMFS. The pathological channel properties of this mutation and its effect on neuronal excitability were investigated. Additionally, this study aimed to develop a medication for effective prevention of KCNT1 mutation-induced seizures. Experimental Approach Wild-type or mutant KCNT1 plasmids were expressed heterologously in Xenopus laevis oocytes, and channel property assessment and drug screening were performed based on two-electrode voltage-clamp recordings. The single-channel properties were investigated using the excised inside-out patches from HEK293T cells. Through in utero electroporation, WT and M267T Slack channels were expressed in the hippocampal CA1 pyramidal neurons in male mice, followed by the examination of the electrical properties using the whole-cell current-clamp technique. The kainic acid-induced epilepsy model in male mice was used to evalute the antiseizure effects of carvedilol. Key Results The KCNT1 M267T mutation enhanced Slack channel function by increasing single-channel open probability. Through screening 16 FDA-approved ion channel blockers, we found that carvedilol effectively reversed the mutation-induced gain-of-function channel properties. Notably, the KCNT1 M267T mutation in the mouse hippocampal CA1 pyramidal neurons affected afterhyperpolarization properties and induced neuronal hyperexcitability, which was inhibited by carvedilol. Additionally, carvedilol exhibited antiseizure effects in the kainic acid-induced epilepsy model. Conclusion and Implication Our findings suggest carvedilol as a new potential candidate for treatment of epilepsies. Graphical
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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医学遗传学
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DOI
PubMed
高影响因子
BRITISH JOURNAL OF PHARMACOLOGY
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2024
·
IF 6.8
Yun Zhao,Guobin Zheng,Shu Yang,Shangjing Liu,Yifan Wu,Yaodong Miao,Zhen Liang,Yunqing Hua,Jing Zhang,Jia Shi,Dan Li,Yanfei Cheng,Yunsha Zhang,Yuanli Chen,Guanwei Fan,Chuanrui Ma
Background and purpose Atherosclerosis is the basis of cardiovascular disease. Ferroptosis is a form of programmed cell death characterized by lipid peroxidation, which contributes to atherogenesis. The plant extract PNS ( Panax notoginseng saponins ), containing the main active ingredients of Panax notoginseng , exhibits anti-atherogenic properties. Herein, we determined whether PNS and its major components could attenuate atherosclerosis by suppressing ferroptosis and revealed the underlying mechanism(s). Experimental approach The anti-atherogenic effects of PNS and their association with inhibition of ferroptosis was determined in apoE −/− mice. In vitro, the anti-ferroptotic effect and mechanism(s) of PNS components were demonstrated in the presence of ferroptosis inducers. Expression of ferroptosis markers and the ubiquitination of Keap1 were evaluated in USP2 −/− macrophages. Finally, the anti-atherogenic effect of USP2 knockout was determined by using USP2 −/− mice treated with high-fat diet (HFD) and AAV-PCSK9. Key results PNS inhibited ferroptosis and atherosclerosis in vivo. PNS suppressed ferroptosis and ferroptosis-aggravated foam cell formation and inflammation in vitro. Mechanistically, PNS and its components activated Nrf2 by antagonizing Keap1, which was attributed to the inhibition of USP2 expression. USP2 knockout antagonized ferroptosis and ferroptosis-aggravated foam cell formation and inflammation, thus mitigating atherosclerosis. USP2 knockout abolished inhibitory effects of PNS on foam cell formation and inflammation in vitro. Conclusion and implications PNS reduced USP2-mediated Keap1 de-ubiquitination and promoted Keap1 degradation, thereby activating Nrf2, improving iron metabolism and reducing lipid peroxidation, thus contributing to an anti-atherosclerotic outcome. Our study revealed the mechanism(s) underlying inhibition of ferroptosis and atherosclerosis by PNS. Graphical
研究领域:
心血管疾病
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药理学
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细胞生物学
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分子生物学
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DOI
PubMed
高影响因子
BRITISH JOURNAL OF PHARMACOLOGY
·
2024
·
IF 6.8
Huilin Liu,Chao Huang,Zhenni Liu,Yuhan Li,Yanan Zhu,Min Gao,Jing Chen,Hui Zhang,Zhengtao Xiao,Wei Zhao
Background and Purpose Cardiac glycosides (CGs), traditionally prescribed for heart failure and arrhythmias, show anticancer potential. However, their mechanisms for preferential inhibition of tumour tissue and constituent malignant cells are not fully elucidated. This study aims to elucidate the therapeutic benefits of CGs in targeting specific tumours and dissect their multi-targeting mechanisms that confer their cytotoxicity against malignant cells. Experimental Approach We designed an integrated workflow to identify therapeutic CGs with high toxicity to certain cancers, investigating their multi-target effects, assessing their toxicity to malignant cells and analysing the prognostic relevance of CGs' target genes. The computational findings were confirmed through gene knockdown, cell viability assays, reactive oxygen species (ROS) measurements and so forth. Key Results CGs modulate multiple genes crucial for ion homeostasis, oxidative stress and apoptosis, with a particularly strong inhibitory effects on uveal melanoma (UVM). Notably, digitoxin suppresses UVM cell proliferation and induces ROS levels by simultaneously targeting STAT3 and KLF5. Single-cell transcriptomic analysis revealed that malignant cells are likely more vulnerable to CGs due to their higher expression of CG target genes compared with surrounding cells in the UVM microenvironment. Conclusions and Implications Given UVM's limited options, our study highlights the potential of digitoxin as a promising novel therapeutic agent for this aggressive and rare ocular cancer. Our comprehensive approach is effective in identifying the potent, cancer-specific therapeutic agents from herbal plants.
研究领域:
肿瘤学
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药理学
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分子生物学
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DOI
PubMed
高影响因子
BRITISH JOURNAL OF PHARMACOLOGY
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2025
·
IF 7.7
Yiling Mei,Xudong Chen,Si Shi,Wante Lin,Zhenfeng Cheng,Xiaoxi Fan,Wenqi Wu,Jibo Han,Weijian Huang,Bozhi Ye,Shanshan Dai
Background and Purpose Myocardial dysfunction is a significant complication associated with sepsis. However, there are currently no specific and effective treatments available. Inhibiting gasdermin D (GSDMD)-mediated pyroptosis has shown promise in mitigating sepsis-induced myocardial dysfunction. The GSDMD inhibitor Y2 (GI-Y2) has been demonstrated to directly bind to GSDMD. Nonetheless, it remains uncertain whether GI-Y2 offers a cardioprotective effect in the context of sepsis-induced myocardial dysfunction. Experimental Approach A mouse model of sepsis was created using lipopolysaccharide (LPS), caecal ligation and puncture. Following treatment with GI-Y2 or macrophage membrane-encapsulated GI-Y2 nanoparticles (GI-Y2@MM-NPs), myocardial dysfunction and pyroptosis levels in heart tissues were assessed. Transcriptome sequencing revealed the molecular mechanism of GI-Y2 in treating septic cardiomyopathy. Key Results We observed that GI-Y2 alleviated myocardial dysfunction and attenuated cardiac inflammation in mice induced by LPS, caecal ligation and puncture. GI-Y2 reduced macrophage pyroptosis and attenuated macrophage-mediated cardiomyocyte injury induced by LPS/nigericin. Concurrently, we confirmed the protective effect of GI-Y2 against LPS-induced cardiac dysfunction was abolished in the absence of GSDMD. Additionally, GI-Y2 attenuated the mitochondrial damage induced by LPS by inhibiting GSDMD in the mitochondria. Furthermore, we developed GI-Y2@MM-NPs to enhance the targeting capability of GI-Y2 towards macrophages in heart tissues and demonstrated its protective effect in vivo . Conclusion and Implications These findings indicate that GI-Y2 alleviates septic myocardial injury and dysfunction by specifically targeting GSDMD, thereby inhibiting GSDMD-mediated pyroptosis and mitochondrial damage. Both GI-Y2 and GI-Y2@MM-NPs may serve as promising therapeutic options for addressing septic myocardial dysfunction. Graphical
研究领域:
免疫学
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心脏病学
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药理学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
BRITISH JOURNAL OF PHARMACOLOGY
·
2024
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IF 6.8
Yun Wang,Jiawei Wu,Yu Hong,Jiaying Zhu,Youcai Zhang,Jun Zhang,Chujie Ding,Yuan Che,Guangji Wang,Aiqin Jiang,Haiping Hao,Lijuan Cao
Background and Purpose Panax ginseng is widely applied in the adjuvant treatment of cardiometabolic diseases in clinical practice without clear mechanisms. This study aims to clearly define the efficacy and underlying mechanism of P. ginseng and its active components in protecting against atherosclerosis. Experimental Approach The anti-atherogenic efficacy of total ginseng saponin extract (TGS) and its components was evaluated on Ldlr −/− mice. Gut microbial structure was analysed by 16S rRNA sequencing and PCR. Bile acid profiles were revealed using targeted metabolomics with LC–MS/MS analysis. The contribution of gut microbiota to atherosclerosis was assessed by co-housing experiments. Key Results Ginsenoside Rb1, representing protopanaxadiol (PPD)-type saponins, increased intestinal Lactobacillus abundance, resulting in enhanced bile salt hydrolase (BSH) activity to promote intestinal conjugated bile acid hydrolysis and excretion, followed by suppression of enterohepatic farnesoid X receptor (FXR)–fibroblast growth factor 15 (FGF15) signal, and thereby increased cholesterol 7α-hydroxylase (CYP7A1) transcriptional expression and facilitated metabolic elimination of cholesterol. Synergistically, protopanaxatriol (PPT)-type saponins, represented by ginsenoside Rg1, protected against atherogenesis-triggered gut leak and metabolic endotoxaemia. Ginsenoside Rg1 directly induced mucin production to nutritionally maintain Akkermansia muciniphila , which reciprocally inhibited gut permeation. Rb1/Rg1 combination, rather than a single compound, can largely mimic the holistic efficacy of TGS in protecting Ldlr −/− mice from atherogenesis. Conclusion and Implications Our study provides strong evidence supporting TGS and ginsenoside Rb1/Rg1 combinations as effective therapies against atherogenesis, via targeting different signal nodes by different components and may provide some elucidation of the holistic mode of herbal medicines.
研究领域:
药理学
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心血管疾病
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微生物学
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代谢组学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
BRITISH JOURNAL OF PHARMACOLOGY
·
2025
·
IF 7.7
Huan Li,Chang Chen,Xinzhu Chen,Jiale Liu,Chen Luo,Huilin Chen,Xiaoyu Geng,Zheng Pan
Background and Purpose We previously showed that the iridoid glycoside extract of Lamiophlomis rotata (IGLR) induces M2 macrophage polarisation to accelerate wound healing. The potentially active compounds (quality markers) in IGLR that accelerate wound healing have not been elucidated; we here identified quality markers that accelerate wound healing. Experimental Approach After IGLR gavage of dorsal excisional wound mice and normal mice for 7 days, the tissues were analysed using the matrix-assisted laser desorption/ionisation (MALDI) mass spectrometry imaging (MSI) method and were further validated by liquid chromatography/mass spectrometry (LC/MS) coupled with multivariate analyses to identify quality markers. Key Results Using the MSI assay, Shanzhiside methyl ester (SM), 8- O -acetylshanzhiside methyl ester (ASM) and Phlorigidoside C (PhC) were identified as the quality markers in IGLR and overlapped with endogenous metabolites (lactate, citrate and itaconate) in the same class by UMAP manifold analysis. Additionally, the results were also confirmed by UPLC-Q/TOF-MS coupled with multivariate analyses of the skin tissues in normal and wound groups. MSI data from the livers and kidneys revealed that the accumulation of SM, ASM and PhC in the livers significantly increased in the model group, and the ion intensity of their glucuronide conjugates in the kidneys was decreased compared to the normal group. These results suggested that bioavailability of these compounds was improved in the wound group. Conclusions and Implications The overall data demonstrated that SM, ASM and PhC were selectively increased in new granulation tissues, and are most likely the quality markers that accelerate wound healing. Graphical
研究领域:
药理学
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分子生物学
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分析化学
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产品关联
DOI
PubMed
高影响因子
BRITISH JOURNAL OF PHARMACOLOGY
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2024
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IF 6.8
Chen Pan,Yuhao Xu,Zongsheng Jiang,Chengjiang Fan,Zhexi Chi,Yu Zhang,Mengmeng Miao,Yuxuan Ren,Ziyi Wu,Linbin Xu,Changqing Mei,Qingge Chen,Yang Xi,Xiaowei Chen
Background and Purpose Chemotherapy-induced peripheral neuropathy (CIPN) commonly causes neuropathic pain, but its pathogenesis remains unclear, and effective therapies are lacking. Naringenin, a natural dihydroflavonoid compound, has anti-inflammatory, anti-nociceptive and anti-tumour activities. However, the effects of naringenin on chemotherapy-induced pain and chemotherapy effectiveness remain unexplored. Experimental Approach Female and male mouse models of chemotherapy-induced pain were established using paclitaxel. Effects of naringenin were assessed on pain induced by paclitaxel or calcitonin gene-related peptide (CGRP) and on CGRP expression in dorsal root ganglia (DRG) and spinal cord tissue. Additionally, we examined peripheral macrophage infiltration, glial activation, c-fos expression, DRG neuron excitability, microglial M1/M2 polarization, and phosphorylation of spinal NF- κ B. Furthermore, we investigated the synergic effect and related mechanisms of naringenin and paclitaxel on cell survival of cancer cells in vitro. Key Results Systemic administration of naringenin attenuated paclitaxel-induced pain in both sexes. Naringenin reduced paclitaxel-enhanced CGRP expression in DRGs and the spinal cord, and alleviated CGRP-induced pain in naïve mice of both sexes. Naringenin mitigated macrophage infiltration and reversed paclitaxel-elevated c-fos expression and DRG neuron excitability. Naringenin decreased spinal glial activation and NF- κ B phosphorylation in both sexes but influenced microglial M1/M2 polarization only in females. Co-administration of naringenin with paclitaxel enhanced paclitaxel's anti-tumour effect, impeded by an apoptosis inhibitor. Conclusion and Implications Naringenin's anti-nociceptive mechanism involves CGRP signalling and neuroimmunoregulation. Furthermore, naringenin facilitates paclitaxel's anti-tumour action, possibly involving apoptosis. This study demonstrates naringenin's potential as a supplementary treatment in cancer therapy by mitigating side effects and potentiating efficacy of chemotherapy. Graphical ∎
研究领域:
药理学
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神经科学
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肿瘤学
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疼痛研究
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产品关联
DOI
PubMed
高影响因子
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