Neuroprotective potential of Honokiol in ICV-STZ induced neuroinflammation, Aβ (1−42) and NF-kB expression in experimental model of rats

Singh, Lovekesh; Singh, Shamsher

doi:10.1016/j.neulet.2023.137090

Cited by 14 publications

(2 citation statements)

References 25 publications

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“… 19 Besides, significantly suppressed Aβ plaque formation, neuroinflammation and neuronal loss have been discovered in AD rats treated with HKL. 20 Thus, all of these previous findings suggest the neuroprotective function and therapeutic effect of HKL on AD. However, the exact molecular mechanisms by which HKL treats AD remain unelucidated to fully support its clinical application.…”

Section: Introductionmentioning

confidence: 83%

Honokiol relieves hippocampal neuronal damage in Alzheimer's disease by activating the SIRT3‐mediated mitochondrial autophagy

Li,

Sun,

et al. 2024

CNS Neurosci Ther

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BackgroundThis work elucidated the effect of honokiol (HKL) on hippocampal neuronal mitochondrial function in Alzheimer's disease (AD).MethodsAPP/PS1 mice were used as AD mice models and exposed to HKL and 3‐TYP. Morris water maze experiment was performed to appraise cognitive performance of mice. Hippocampal Aβ+ plaque deposition and neuronal survival was evaluated by immunohistochemistry and Nissl staining. Hippocampal neurons were dissociated from C57BL/6 mouse embryos. Hippocampal neuronal AD model was constructed by Aβ oligomers induction and treated with HKL, CsA and 3‐TYP. Neuronal viability and apoptosis were detected by cell counting kit‐8 assay and TUNEL staining. mRFP–eGFP–LC3 assay, MitoSOX Red, dichlorodihydrofluorescein diacetate, and JC‐1 staining were performed to monitor neuronal autophagosomes, mitochondrial reactive oxygen species (ROS), neuronal ROS, and mitochondrial membrane potential. Autophagy‐related proteins were detected by Western blot.ResultsIn AD mice, HKL improved cognitive function, relieved hippocampal Aβ1–42 plaque deposition, promoted hippocampal neuron survival, and activated hippocampal SIRT3 expression and mitochondrial autophagy. These effects of HKL on AD mice were abolished by 3‐TYP treatment. In hippocampal neuronal AD model, HKL increased neuronal activity, attenuated neuronal apoptosis and Aβ aggregation, activated SIRT3 and mitochondrial autophagy, reduced mitochondrial and neuronal ROS, and elevated mitochondrial membrane potential. CsA treatment and 3‐TYP treatment abrogated the protection of HKL on hippocampal neuronal AD model. The promotion of mitochondrial autophagy by HKL in hippocampal neuronal AD model was counteracted by 3‐TYP.ConclusionsHKL activates SIRT3‐mediated mitochondrial autophagy to mitigate hippocampal neuronal damage in AD. HKL may be effective in treating AD.

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Section: Introductionmentioning

confidence: 83%

Honokiol relieves hippocampal neuronal damage in Alzheimer's disease by activating the SIRT3‐mediated mitochondrial autophagy

Li,

Sun,

et al. 2024

CNS Neurosci Ther

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“…Microglia are CNS immune cells that can protect neurons by phagocytosing pathogens and harmful particles in the brain tissue and can also activate reactive microglia that secrete inflammatory cytokines in response to inflammatory factors, resulting in neuronal toxicity [ 28 , 29 ]. Therefore, reactive microglia are an important target for treating neuroinflammation and NDs [ 30 ]. LPS, a glycolipid composed of lipids and polysaccharides, is a constituent of the outer wall of gram-negative bacterial cell walls [ 31 , 32 ].…”

Section: Discussionmentioning

confidence: 99%

Libertellenone C attenuates oxidative stress and neuroinflammation with the capacity of NLRP3 inhibition

Cao,

Li,

Zhang

et al. 2024

Nat. Prod. Bioprospect.

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Neurodegenerative diseases (NDs) are common chronic diseases arising from progressive damage to the nervous system. Here, in-house natural product database screening revealed that libertellenone C (LC) obtained from the fermentation products of Arthrinium arundinis separated from the gut of a centipede collected in our Tongji campus, showed a remarkable neuroprotective effect. Further investigation was conducted to clarify the specific mechanism. LC dose-dependently reversed glutamate-induced decreased viability, accumulated reactive oxygen species, mitochondrial membrane potential loss, and apoptosis in SH-SY5Y cells. Network pharmacology analysis predicted that the targets of LC were most likely directly related to oxidative stress and the regulation of inflammatory factor-associated signaling pathways. Further study demonstrated that LC attenuated nitrite, TNF-α, and IL-1β production and decreased inducible nitric oxide synthase and cyclooxygenase expression in lipopolysaccharide-induced BV-2 cells. LC could directly inhibit NLRP3 inflammasome activation by decreasing the expression levels of NLRP3, ASC, cleaved Caspase-1, and NF-κB p65. Our results provide a new understanding of how LC inhibits the NLRP3 inflammasome in microglia, providing neuroprotection. These findings might guide the development of effective LC-based therapeutic strategies for NDs.

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Herbal Approaches for the Management of Neurological Disorders

Yadav,

Guin,

Nayak

et al. 2023

Drug Delivery Strategies in Neurological Disorders: Challenges and Opportunities

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Neuroprotective potential of Honokiol in ICV-STZ induced neuroinflammation, Aβ (1−42) and NF-kB expression in experimental model of rats

Cited by 14 publications

References 25 publications

Honokiol relieves hippocampal neuronal damage in Alzheimer's disease by activating the SIRT3‐mediated mitochondrial autophagy

Honokiol relieves hippocampal neuronal damage in Alzheimer's disease by activating the SIRT3‐mediated mitochondrial autophagy

Libertellenone C attenuates oxidative stress and neuroinflammation with the capacity of NLRP3 inhibition

Herbal Approaches for the Management of Neurological Disorders

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