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Honokiol alleviates the degeneration of intervertebral disc via suppressing the activation of TXNIP-NLRP3 inflammasome signal pathway.

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Intervertebral disc degeneration (IVDD) is a multifactorial disease and responsible for many spine related disorders, causes disability in the workforce and heavy social costs all over the world. Honokiol, a low molecular weight natural product, could penetrate into and distribute in IVDs to achieve

Protective and therapeutic activity of honokiol in reversing motor deficits and neuronal degeneration in the mouse model of Parkinson's disease.

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BACKGROUND Parkinson's disease (PD) is a progressive and profound movement disorder resulting from neurodegeneration in the nigrostriatal dopaminergic system, but current treatment neither cures nor stops PD from advancing. Based on the ability to suppress oxidative stress, excitotoxicity, and

Honokiol for the Treatment of Neonatal Pain and Prevention of Consequent Neurobehavioral Disorders.

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This study examined the short- and long-term neuroprotective and analgesic activity of honokiol (a naturally occurring lignan isolated from Magnolia) on developing brains in neonates exposed to inflammatory pain, known to cause neuronal cell death. Postnatal day 4 (P4) neonatal rat pups were

Honokiol protects osteoblastic MC3T3-E1 cells against antimycin A-induced cytotoxicity.

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OBJECTIVE Honokiol is a phenolic compound isolated from the bark of Magnolia officinalis, a plant widely used in traditional medicine. Antimycin A, which inhibits complex III of the electron transport system, has been used as a reactive oxygen species generator in biological systems. In the present

Protective effects of honokiol on ischemia/reperfusion injury of rat ovary: an experimental study.

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OBJECTIVE The purpose of this study was to investigate the protective effect of honokiol on experimental ischemia/reperfusion injury of rat ovary. METHODS A total of 40 female Wistar albino rats were used in this study. The rats were divided into five groups as follows: sham (Group I), torsion

Intravenous administration of Honokiol provides neuroprotection and improves functional recovery after traumatic brain injury through cell cycle inhibition.

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Recently, increasing evidence has shown that cell cycle activation is a key factor of neuronal death and neurological dysfunction after traumatic brain injury (TBI). This study aims to investigate the effects of Honokiol, a cell cycle inhibitor, on attenuating the neuronal damage and facilitating

Honokiol Protects against Anti-β1-Adrenergic Receptor Autoantibody-Induced Myocardial Dysfunction via Activation of Autophagy.

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Myocardial diseases are prevalent syndromes with high mortality rate. The exploration of effective interference is important. Anti-β1-adrenergic receptor autoantibody (β1-AAB) is highly correlated with myocardial dysfunction. The actions and underlying mechanisms of honokiol (HNK) in β1-AAB-positive

Acute and sub-chronic toxicity studies of honokiol microemulsion.

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The purpose of this study was to investigate the acute and sub-chronic toxicity of honokiol microemulsion. In the acute toxicity tests, the mice were intravenously injected graded doses of honokiol microemulsion and were observed for toxic symptoms and mortality daily for 14 days. In the sub-chronic

Expression of VEGF and GFAP in a rat model of traumatic brain injury treated with Honokiol: a biochemical and immunohistochemical study.

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Traumatic brain injury leads to neuronal damage and neurological dysfunction. The aim of our study was to investigate the antioxidative effect of Honokiol on traumatic brain injury in rats with biochemical, histopathological and immunohistochemical methods. Sprague-Dawley rats were subjected to

Honokiol attenuates torsion/detorsion-induced testicular injury in rat testis by way of suppressing endoplasmic reticulum stress-related apoptosis.

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OBJECTIVE To investigate the protective effect of honokiol, a phytochemical used in traditional medicine, on testicular injury after torsion/detorsion (T/D) in a rat model. Testicular torsion is a medical emergency that can cause impairment of semen quality and permanent testicular atrophy or

Honokiol stimulates osteoblastogenesis by suppressing NF-κB activation.

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Magnolia officinalis, a component of Asian herbal teas, has long been employed in traditional Japanese and Chinese medicine to treat numerous maladies. Honokiol, a biphenolic compound, is now considered to be one of the major active ingredients of Magnolia extract, and is under intense investigation

Honokiol suppresses mycelial growth and reduces virulence of Botrytis cinerea by inducing autophagic activities and apoptosis.

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Fungal pathogens lead to severe quality deterioration and yield loss, making it urgent to explore efficient measures to control fungal diseases at the preharvest and postharvest stages of plants. Therefore, studies on natural substances targeting alternative antimicrobial targets have become hot

In vitro Penetration and in vivo Distribution of Honokiol into the Intervertebral Disc in Rat.

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Honokiol is a potential candidate for the treatment of intervertebral disc (IVD) degeneration. In this study, we develop in vitro and in vivo methods to detect the distribution of honokiol in intervertebral discs using high-performance liquid chromatography. A rat tail disc was used for both

Small molecule natural compound agonist of SIRT3 as a therapeutic target for the treatment of intervertebral disc degeneration.

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Oxidative stress-induced mitochondrial dysfunction is implicated in the pathogenesis of intervertebral disc degeneration (IVDD). Sirtuin 3 (SIRT3), a sirtuin family protein located in mitochondria, is essential for mitochondrial homeostasis; however, the role of SIRT3 in the process of IVDD has

SIRT3-Dependent Mitochondrial Dynamics Remodeling Contributes to Oxidative Stress-Induced Melanocyte Degeneration in Vitiligo.

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Mitochondrial dysregulation has been implicated in oxidative stress-induced melanocyte destruction in vitiligo. However, the molecular mechanism underlying this process is merely investigated. Given the prominent role of nicotinamide adenine dinucleotide (NAD⁺)-dependent deacetylase

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