Identification of the natural chalcone glycoside hydroxysafflor yellow A as a suppressor of P53 overactivation‐associated hematopoietic defects DOI Creative Commons
Jing Chen, Can Ren, Chong Yao

et al.

MedComm, Journal Year: 2023, Volume and Issue: 4(5)

Published: Aug. 24, 2023

Abstract Enhanced P53 signaling may lead to hematopoietic disorders, yet an effective therapeutic strategy is still lacking. Our study, along with previous research, suggests that overactivation and defects are major consequences of zinc deficiency. However, the relationship between these two pathological processes remains unclear. In this we observed a severe reduction in number stem cells (HSCs) multi‐lineage progenitor zebrafish treated chelator N , ′, ′‐tetrakis(2‐pyridylmethyl)ethylenediamine showed indispensable role process. Next, took advantage HSCs‐labeled transgenic conducted highly efficient phenotypic screening for small molecules against P53‐dependent disorders. Hydroxysafflor yellow A (HSYA), natural chalcone glycoside, exhibited potent protection failure zinc‐deficient strongly inhibited pathway. We confirmed protective effect HSYA mice bone marrow nucleated cells, which significant suppression oxidative stress. Furthermore, hematopoietic‐protective activity was validated using model myelotoxicity induced by 5‐FU. summary, our work provides identifying agents reveals novel as promising compound rescuing disorders associated overactivation.

Language: Английский

Combination therapies and other therapeutic approaches targeting the NLRP3 inflammasome and neuroinflammatory pathways: a promising approach for traumatic brain injury DOI

Zana Montazeri-Khosh,

Ahmad Ebrahimpour, Mina Keshavarz

et al.

Immunopharmacology and Immunotoxicology, Journal Year: 2025, Volume and Issue: unknown, P. 1 - 17

Published: Jan. 6, 2025

Objectives: Traumatic brain injury (TBI) precipitates a neuroinflammatory cascade, with the NLRP3 inflammasome emerging as critical mediator. This review scrutinizes complex activation pathways of by underscoring intricate interplay between calcium signaling, mitochondrial disturbances, redox imbalances, lysosomal integrity, and autophagy. It is hypothesized that combination therapy approach—integrating NF-κB pathway inhibitors antagonists—holds potential to synergistically dampen inflammatory storm associated TBI.

Language: Английский

Citations

2
Metabolomics integrated with network pharmacology of blood-entry constituents reveals the bioactive component of Xuefu Zhuyu decoction and its angiogenic effects in treating traumatic brain injury DOI Creative Commons
Teng Li,

Lianglin Zhang,

Menghan Cheng

et al.

Chinese Medicine, Journal Year: 2024, Volume and Issue: 19(1)

Published: Sept. 26, 2024

Language: Английский

Citations

10
The role of astrocyte in neuroinflammation in traumatic brain injury DOI Creative Commons
Liang He, Ruqiang Zhang,

Maiqiao Yang

et al.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Journal Year: 2023, Volume and Issue: 1870(3), P. 166992 - 166992

Published: Dec. 19, 2023

Language: Английский

Citations

13
The neuroprotective potential of phytochemicals in traumatic brain injury: mechanistic insights and pharmacological implications DOI Creative Commons
Gulam Mustafa Hasan,

Saleha Anwar,

Anas Shamsi

et al.

Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 14

Published: Jan. 4, 2024

Traumatic brain injury (TBI) leads to damage, comprising both immediate primary damage and a subsequent cascade of secondary mechanisms. The results in localized while the initiates inflammatory responses, followed by disruption blood-brain barrier, infiltration peripheral blood cells, edema, release various immune mediators, including chemotactic factors interleukins. TBI disrupts molecular signaling, cell structures, functions. In addition physical tissue such as axonal injuries, contusions, haemorrhages, interferes with functioning, impacting cognition, decision-making, memory, attention, speech capabilities. Despite deep understanding pathophysiology TBI, an intensive effort evaluate underlying mechanisms effective therapeutic interventions is imperative manage repercussions TBI. Studies have commenced explore potential employing natural compounds for These are characterized their low toxicity limited interactions conventional drugs. Moreover, many demonstrate capacity target aspects process. While our there urgent need mitigate its consequences. Here, we aimed summarize mechanism action role phytochemicals against progression. This review discusses implications phytonutrients addresses consequences addition, highlighted roles emerging promising candidates intervention highlights neuroprotective mechanistic approach. Furthermore, efforts focused on mechanisms, providing better therapeutics.

Language: Английский

Citations

5
Interleukin-1 Receptor-Associated Kinase-3 Aggravates Neuroinflammatory Injury After Intracerebral Hemorrhage via Activation NF-κB/IL-17A Pathway in Mice DOI Creative Commons
Jun Wang, Yulong Li, Chunyu Tan

et al.

Journal of Inflammation Research, Journal Year: 2025, Volume and Issue: Volume 18, P. 1167 - 1189

Published: Jan. 1, 2025

Neuroinflammatory reactions are crucial factors in secondary brain damage following intracerebral hemorrhage (ICH). Although previous studies have shown that IRAK3 is involved immune responses, the potential effects of on ICH remain unclear. Collagenase IV-induced mouse model. Western blotting was used to determine expression at different time points ICH. Immunofluorescence investigate cellular localization IRAK3. The model treated with recombinant human (rh-IRAK3) or siRNA via an intracerebroventricular injection. effect mice assessed by and short-term long-term neurological function evaluation. RNA-seq performed explore mechanism which promotes inflammation after mechanisms neuroinflammation will be further investigated blotting, qRT-PCR immunofluorescence. Recombinant IL-17A connection between NF-κB/IL-17A signaling pathway vivo vitro experiments. increased, peaking 24 h, followed a subsequent decrease mainly expressed microglia. analysis revealed 1,797 differentially genes around perihematomal tissue treatment, multiple inflammatory pathways being downregulated. Rh-IRAK3 treatment resulted upregulation levels cytokines exacerbated deficits. Furthermore, markedly decreased microglial activation pathway. response vitro; however, knockdown reversed this process. aggravates activating pathway, thereby exacerbating deficits Therefore, inhibition may promising approach for treating

Language: Английский

Citations

0
Activation of SIRT1 by Hydroxysafflor Yellow A Attenuates Chronic Unpredictable Mild Stress‐Induced Microglia Activation and Iron Death in Depressed Rats DOI Creative Commons

Jianle He,

Min He,

Ping Yang

et al.

Brain and Behavior, Journal Year: 2025, Volume and Issue: 15(3)

Published: March 1, 2025

Hydroxysafflor yellow A (HSYA), the main active ingredient in safflower, possesses antioxidant and anti-inflammatory activities. We confirmed our previous study that HSYA exerts antidepressant effects, but further investigation is needed to uncover exact mechanism. Herein, we aimed explore effects of based on microglial activation ferroptosis studies. The chronic unpredictable mild stress (CUMS) procedure was used establish a depression model rats. Behavioral tests were conducted rats after administration. Iba-1 immunostaining determine microglia hippocampus. examined iron ion level using colorimetric method. Assayed by western blot for protein expression. Rats receiving showed enhanced spatial learning memory abilities, as well improvements depression-like behaviors. administration reduced expression CUMS rats' hippocampus, indicating suppressed activation. inhibited CUMS-induced Fe2+ concentration promoted ferroptosis-related GPX4 SLC7A11 treatment also elevated SIRT1 Nrf2 levels, while p-p65 levels decreased hippocampus an antidepressant-like effect inhibiting inducing SIRT1/Nrf2/NF-kB signaling.

Language: Английский

Citations

0
Research progress of active compounds from traditional Chinese medicine in the treatment of stroke DOI
Xiaoxing Yin,

Shutang Li,

Junwei Wang

et al.

European Journal of Medicinal Chemistry, Journal Year: 2025, Volume and Issue: unknown, P. 117599 - 117599

Published: April 1, 2025

Language: Английский

Citations

0
Hydrogen combined with needle-embedding therapy alleviates traumatic brain injury by inhibiting NLRP3 inflammasome activation via STING signaling pathway DOI
Fan Wu, Wenting Su, Xin Wang

et al.

Cytokine, Journal Year: 2025, Volume and Issue: 190, P. 156931 - 156931

Published: April 6, 2025

Language: Английский

Citations

0
A Combination of Astragaloside IV and Hydroxysafflor Yellow A Attenuates Cerebral Ischemia-Reperfusion Injury via NF-κB/NLRP3/Caspase-1/GSDMD Pathway DOI Creative Commons

Yongchun Hou,

Zi Yan, Haitong Wan

et al.

Brain Sciences, Journal Year: 2024, Volume and Issue: 14(8), P. 781 - 781

Published: July 31, 2024

Cerebral ischemia-reperfusion injury (IRI), occurring after blood supply restoration, contributes significantly to stroke-related deaths. This study explored the combined impact and mechanisms of astragaloside IV (AS-IV), hydroxysafflor yellow A (HSYA), their combination in mitigating IRI. Male Sprague-Dawley (SD) rats were randomized Sham, MCAO, MCAO+AS-IV, MCAO+HSYA, MCAO+AS-IV+HSYA groups. Neurological deficits cerebral infarction examined restoring brain. Pathomorphological changes cortex observed via HE staining. IL-1β IL-18 quantified using ELISA. The expression NF-κB GSDMD ischemic cerebrum was analyzed immunohistochemistry. levels NLRP3, ASC, IL-1β, Caspase-1, evaluated Western blot. groups exhibited notably better neurological function compared with MCAO group. treatment demonstrated superior brain tissue alleviation. Reductions NF-κB, positive cells, NLRP3/ASC/IL-1β/Caspase-1/GSDMD protein more pronounced therapy, indicating a synergistic effect countering IRI NF-κB/NLRP3/Caspase-1/GSDMD pathway inhibition cell pyroptosis-induced injury.

Language: Английский

Citations

2
The activation of the HIF-1α-VEGFA-Notch1 signaling pathway by Hydroxysafflor yellow A promotes angiogenesis and reduces myocardial ischemia–reperfusion injury DOI Creative Commons

Chaowen Ge,

Dongdong Meng,

Yuqin Peng

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 142, P. 113097 - 113097

Published: Sept. 10, 2024

Language: Английский

Citations

2