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Last update 08 May 2025

NLRP3 x TLR4 x HMGB1

Last update 08 May 2025

Basic Info

Related Targets

NLRP3TLR4HMGB1

Drugs associated with NLRP3 x TLR4 x HMGB1

Acteoside

Target

HMGB1 x NLRP3 x TLR4

Mechanism

HMGB1 inhibitors [+2]

Active Org.

Chinese PLA Academy of Military Medical Sciences [+5]

Originator Org.-

Active Indication

Diabetic Nephropathies [+2]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with NLRP3 x TLR4 x HMGB1

CTRI/2008/091/000247

/ Not yet recruitingPhase 2

COMPARATIVE EVALUATION OF ACTEOSIDE AND SILYMARIN AS HEPATOPROTECTIVE AGENTS IN ACUTE HEPATITIS PATIENTS-A RANDOMIZED PROSPECTIVE OPEN FRAME STUDY

Start Date15 Dec 2008

Sponsor / Collaborator

Government Medical College Jammu

[+1]

100 Clinical Results associated with NLRP3 x TLR4 x HMGB1

100 Translational Medicine associated with NLRP3 x TLR4 x HMGB1

0 Patents (Medical) associated with NLRP3 x TLR4 x HMGB1

120

Literatures (Medical) associated with NLRP3 x TLR4 x HMGB1

01 May 2025·Phytomedicine

Therapeutic efficacy of Xuebijing injection in treating severe acute pancreatitis and its mechanisms of action: A comprehensive survey

Review

Author: Shang, Hongcai ; Jiang, Tong ; Chen, Zhuo ; Zheng, Rui ; Zhang, Xinyi ; Zhang, Xiaowei ; Jiang, Huiru ; Peng, Mengqi

BACKGROUNDSevere acute pancreatitis (SAP) is a life-threatening condition associated with high mortality and limited therapeutic options. Current management strategies focus on infection prevention, immune regulation, and anticoagulation. Xuebijing Injection (XBJ), a widely used traditional Chinese medicine-derived intravenous preparation, has shown promising therapeutic effects in SAP. Herein, we sought to evaluate clinical and preclinical evidence on XBJ to reveal its potential mechanisms of action, and provide insights to guide future research and clinical applications.METHODSWe conducted a comprehensive survey of studies on XBJ in the treatment of SAP across PubMed, Embase, Cochrane Library, CBM, CNKI, Wanfang and VIP databases from their inception to March 21st, 2024.RESULTSA total of 239 studies were included, comprising 12 animal experiments, 7 systematic reviews, 220 clinical trials. Mechanistic studies suggest that XBJ downregulates the expression of inflammatory mediators, improves immune function, and alleviates oxidative stress via multiple signaling pathways, including the TLR4/NF-κB, p38-MAPK, HMGB1/TLR, TLR4/NF-κB, FPR1/NLRP3, and JAK/STAT pathways. These effects contribute to reducing organ damage. Compared to standard treatment, XBJ has more effective at reducing mortality and complications, improving overall clinical outcomes, shortening ventilator use time, and hospital stay in SAP patients.CONCLUSIONSPreclinical evidence and clinical trial data indicated that XBJ can simultaneously regulate inflammatory responses, immune function, microcirculatory disorders, oxidative stress, and apoptosis. However, further research is required to elucidate the specific mechanisms of action, clinical characteristics and safety of XBJ.

01 Feb 2025·International Immunopharmacology

Okra seed polysaccharides mitigate neuroinflammation and cognitive impairment via modulation of Nrf2/HO-1, HMGB1/RAGE/TLR4/NF-κB, NLRP3/Caspase-1, JAK-2/STAT-3, AMPK/SIRT1/m-TOR, PI3K/AKT/CREB/BDNF/TrkB and PERK/CHOP/Bcl-2 axes

Article

Author: Azadi, Parastoo ; Selim, Nabil M ; Gowifel, Ayah M H ; Mohamed, Ehsan K ; Black, Ian ; Nazeam, Jilan A ; Mulamoottil, Varughese A ; Hafez, Shaimaa M ; Hamdan, Ahmed M E ; El Shiekh, Riham A ; Abu-Elfotuh, Karema ; El Hefnawy, Hala Mohamed ; Atwa, Ahmed M

Global healthcare systems are under tremendous strain due to the increasing prevalence of neurodegenerative disorders. Growing data suggested that overconsumption of high-fat/high-carbohydrates diet (HFHCD) is associated with enhanced incidence of metabolic alterations, neurodegeneration, and cognitive dysfunction. Functional foods have gained prominence in curbing metabolic and neurological deficits. Consequently, this study endeavored to explore effects of purified Okra seed polysaccharides (OP) (Abelmoschus esculentus (L.) Moench) against HFHCD-induced metabolic alterations and cognitive dysfunction, with elucidating underlying contributed mechanistic pathways. OP hydrolysate was analyzed using GC-MS analysis. The biological study encompassed two phases, the first phase I (model establishment phase), for 3 months, involved a control group, fed standard diet, and HFHCD group. The second phase (phase II) where HFHCD fed rats were re-divided into 3 equal subgroups, 1st subgroup received HFHCD, whereas second and third subgroups received OP, 200 or 400 mg/kg/day, respectively, for 28 days. GC-MS characterized OP as an arabinogalactouranan and revealed the monosaccharide composition as galacturonic acid: arabinose: glucose: galactose: rhamnose: xylose in ratio of 28.2: 23.3: 11.5: 4.2: 3.5: 2.0. The findings demonstrated that OP dose-dependently mitigated HFHCD-induced rise in body weights, lipid profiles, levels of blood glucose and disruption in behavioral outcomes, neurotransmitters, together with histopathological alterations in brain. Moreover, OP dose-dependently improved redox, neuroinflammatory, endoplasmic reticulum (ER) stress, autophagic and apoptotic biomarkers. OP can be regarded as promising functional food candidate to hamper HFHCD-induced metabolic alterations and cognitive deficit, via enhancing Nrf2/HO-1, AMPK/SIRT1 and PI3K/AKT/CREB axes, long with dampening of HMGB1/RAGE/TLR4, NLRP3/Caspase-1, JAK-2/STAT-3 and PERK/CHOP axes.

01 Feb 2025·International Immunopharmacology

Scopoletin alleviates acetaminophen-induced hepatotoxicity through modulation of NLRP3 inflammasome activation and Nrf2/HMGB1/TLR4/NF-κB signaling pathway

Article

Author: Wu, Di ; Yuan, Haidan ; Li, Hui ; Yuan, Yilin ; Piao, Guangchun ; Zhang, Jianxiu ; Cui, Qinglong ; Yuan, Fengxia

Scopoleitin (SP), a bioactive compound from many edible plants and fruits, exerts a wide range of biological activities, however the role and mechanism of SP in acetaminophen (APAP)-induced hepatotoxicity remains unclear. In this study, we verified the protective effect of SP on APAP-induced liver injury (AILI) hepatotoxicity and explore the underlying molecular mechanisms. Here, we showed that SP alleviated AILI by reducing serum alanine transaminase (ALT) and aspartate aminotransferase (AST) levels, hepatic histopathological damage, inflammation, and liver cell apoptosis. In addition, SP attenuated the accumulation of malondialdehyde (MDA) and exhaustion of glutathione (GSH) levels and increased the superoxide dismutase (SOD) levels induced by APAP. Consistently, SP significantly reduced the gene transcription of cytochrome P450 (CYP)2E1, CYP1A2, and CYP3A11 in the livers of mice induced by APAP. Moreover, SP pretreatment effectively promoted the expression of Nrf2, Keap1, and its signal downstream HO-1, NQO1, GCLc, and GCLm, suggesting the activation of the Nrf2 signaling pathway. SP inhibited APAP-induced hepatocyte apoptosis by regulating the protein levels of apoptosis-related proteins (cytochrome C, Bax, Caspase-3, Bcl2, and PARP). SP suppressed APAP-induced expression of NLRP3 and reduced the levels of proinflammatory factors, including tumor necrosis factor-alpha (TNF-α), F4/80, Caspase-1, and interleukin (IL)-1 beta (IL-1β). Moreover, SP downregulated APAP-induced high-mobility group box 1 (HMGB1) and toll-like receptor 4 (TLR4) expression, inhibited nuclear factor kappa-B (NF-κB) and MAPK activation. Taken together, our study reveals the protective roles of SP against AILI through the downregulation of NLRP3 expression, and the inhibition of the Nrf2/HMGB1/TLR4/NF-κB signaling pathways.

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