Neuroprotection of Chikusetsu saponin V on transient focal cerebral ischemia/reperfusion and the underlying mechanism

Zhang, Tiejun; Li, Zhengjun; Zhou, Qin; Cao, Yi; Shan, Tikun; Yuan, Fang; Tang, Lin; Jia, Na; Jia, Jinru; Jin, Zhaohui; Xu, Ting; Li, Yuwen

doi:10.1016/j.phymed.2021.153516

Cited by 11 publications

(4 citation statements)

References 25 publications

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“…JNK has been shown to modulate FoxO3a activity in many ways [ 31 ], while FoxO3a, a subfamily of the FoxO family discovered in recent years, participates in many pathophysiological processes in vivo, including regulating apoptosis, oxidative stress, and energy metabolism [ 32 ]. When focal cerebral ischemia occurs, there will be infiltration of the white blood cells and brain cells (neurons and glia), release of various inflammatory mediators including various cytokines, and production of excessive ROS, resulting in tissue damage [ 33 ]. Reducing inflammatory mediators and releasing and controlling oxidative stress through drug action are commonly used to alleviate focal cerebral ischemia.…”

Section: Discussionmentioning

confidence: 99%

Influence of Melatonin on Behavioral and Neurological Function of Rats with Focal Cerebral Ischemia-Reperfusion Injury via the JNK/FoxO3a/Bim Pathway

Chen

Shen

Lai

et al. 2022

Computational and Mathematical Methods in Medicine

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Objective. To investigate the influence of melatonin on behavioral and neurological function of rats with focal cerebral ischemia-reperfusion injury via the JNK/FoxO3a/Bim pathway. Methods. One hundred and twenty healthy male SD rats were randomized into the model group (Model: the middle cerebral artery occlusion (MCAO) model was constructed and received an equal volume of normal saline containing 5% DMSO), sham operation group (Sham: received no treatment except normal feeding), and low, medium, and high dose of melatonin group (L-MT, M-MT, and H-MT intraperitoneally injected 10, 20, and 40 mg/kg melatonin 30 min after IR, respectively), with 24 rats in each group. Following 24 h of reperfusion, the rats in each of the above groups were tested for neurological deficit symptoms and behavioral changes to screen the rats included in the study. HE and TUNEL stainings were performed to observe pathological changes. Levels of oxidative stress-related indexes, inflammatory factor-related indexes, nuclear factor-κB p65 (NF-κB p65), and interferon-γ (IFN-γ) in the rat brain were measured by ELISA. The JNK/FoxO3a/Bim pathway-related proteins as well as Bcl-2, Caspase-3, and Bax were examined using Western blot. Results. Detection of behavioral indicators showed that the MACO model was successfully constructed in rats. L-MT, M-MT, and L-MT groups presented reduced malondialdehyde (MDA), reactive oxygen species (ROS), tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, IL-1β, IFN-γ, NF-κB p65, and apoptosis compared with the Model group ( P < 0.05 ), and the improvement degree was better in the M-MT group versus the L-HT group. Bcl-2 protein expression in the brain tissue of L-MT, M-MT, and H-MT groups increased significantly, while Bax, Caspase-3, p-JNK, p-FoxO3a, and Bim protein expression declined markedly, versus the Model group ( P < 0.05 ). The changes of indexes were greater in the M-MT group compared with that in the L-MT group. No significant difference was observed in all the above indexes between the M-MT group and the H-MT group ( P > 0.05 ). Conclusions. In the MACO rat model, melatonin can effectively reduce Bax and Caspase-3 levels by modulating the JNK/FoxO3a/Bim pathway, inhibit neuronal apoptosis, and alleviate neurological deficits by reducing the release of proinflammatory mediators, with anti-inflammatory and antioxidant effects. In addition, 20 mg/kg is the optimal melatonin concentration.

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Section: Discussionmentioning

confidence: 99%

Influence of Melatonin on Behavioral and Neurological Function of Rats with Focal Cerebral Ischemia-Reperfusion Injury via the JNK/FoxO3a/Bim Pathway

Chen

Shen

Lai

et al. 2022

Computational and Mathematical Methods in Medicine

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“…For instance, ephedrine and galuteolin have been found to inhibit autophagy ( Zhu et al, 2020 ; Shi et al, 2021 ). Vitexin, puerarin, and alphaasarone have been reported to reduce neuronal autophagy by decreasing Beclin1 expression and the LC3II/LC3I ratio, thus mitigating autophagic activity, while astragaloside IV and nicotiflorin could enhance autophagy and reduce neuronal apoptosis by increasing LC3II/LC3I ratio ( Hongyun et al, 2017 ; Jiang et al, 2018 ; Zhang et al, 2019a ; Zhang et al, 2021a ; Wang et al, 2021b ). In addition, TCM monomers preconditioning could also reduce autophagy in CIRI.…”

Section: Protective Mechanism Of Traditional Chinese Medicine Monomer...mentioning

confidence: 99%

“…Another study found that low-dose curcumin (100 mg/kg in vivo , 5 µM in vitro ) could improve mitochondrial function, increase LC3 II, mitochondrial marker VDAC1 colocalization, LC3-II/LC3-I ratio, and enhance mitophagy ( Wang and Xu, 2020 ). Chikusetsu saponin V (50 mg/kg in vivo , 50 μM in vitro ) reduced deacetylation of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) through AMPK/SIRT-1 pathway, downregulated ROS and maintained mitochondrial respiration ( Zhang et al, 2021b ). In addition, ligustilide (20 mg/kg in vivo , 20 μM in vitro ) promoted DRP1-mediated mitochondrial fission and induced mitophagy by activating AMPK, thereby alleviating CIRI ( Khaksar and Bigdeli, 2017 ).…”

Section: Protective Mechanism Of Traditional Chinese Medicine Monomer...mentioning

confidence: 99%

Role of traditional Chinese medicine monomers in cerebral ischemia/reperfusion injury:a review of the mechanism

Zheng,

Jiang,

Huang

et al. 2023

Front. Pharmacol.

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Ischemia/reperfusion (I/R) injury is a pathological process wherein reperfusion of an ischemic organ or tissue exacerbates the injury, posing a significant health threat and economic burden to patients and their families. I/R triggers a multitude of physiological and pathological events, such as inflammatory responses, oxidative stress, neuronal cell death, and disruption of the blood-brain barrier (BBB). Hence, the development of effective therapeutic strategies targeting the pathological processes resulting from I/R is crucial for the rehabilitation and long-term enhancement of the quality of life in patients with cerebral ischemia/reperfusion injury (CIRI). Traditional Chinese medicine (TCM) monomers refer to bioactive compounds extracted from Chinese herbal medicine, possessing anti-inflammatory and antioxidative effects, and the ability to modulate programmed cell death (PCD). TCM monomers have emerged as promising candidates for the treatment of CIRI and its subsequent complications. Preclinical studies have demonstrated that TCM monomers can enhance the recovery of neurological function following CIRI by mitigating oxidative stress, suppressing inflammatory responses, reducing neuronal cell death and functional impairment, as well as minimizing cerebral infarction volume. The neuroprotective effects of TCM monomers on CIRI have been extensively investigated, and a comprehensive understanding of their mechanisms can pave the way for novel approaches to I/R treatment. This review aims to update and summarize evidence of the protective effects of TCMs in CIRI, with a focus on their role in modulating oxidative stress, inflammation, PCD, glutamate excitotoxicity, Ca2+ overload, as well as promoting blood-brain barrier repairment and angiogenesis. The main objective is to underscore the significant contribution of TCM monomers in alleviating CIRI.

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“…Traditional Chinese Medicine (TCM) active ingredients have attracted increasing attention on their critical biological effects on the progression of various diseases (Dai et al 2021 ; Wei et al 2021 ; Wang et al 2021 ). Some of the monomers of TCM have important neuroprotective effects, such as ginsenoside Rg1 (Yang et al 2020 ), chikusetsu saponin V (Zhang et al 2021 ) and mangiferin (Peng et al 2019 ). For the cognitive impairments induced by sevoflurane, chikusetsu saponin IVa (Shao et al 2020 ) ampelopsin (Liu et al 2020a , b ) and cistanches (Peng et al 2020 ) have been demonstrated to exert beneficial effects on cognitive function by reducing neuroinflammation or improve neuronal cell viability.…”

Section: Introductionmentioning

confidence: 99%

Protective role of trametenolic acid B against sevoflurane-induced cognitive impairments by its different regulatory modalities of mir-329-3p in neurons and microglia

Feng

Qiu

et al. 2022

Mol Med

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Background Postoperative cognitive dysfunction induced by anesthetics commonly occurs in elderly patients. This study aimed to evaluate the protective role of trametenolic acid B (TAB) in sevoflurane-induced cognitive impairments, and explore the underlying mechanisms. Methods Animal and cell experiments were performed in rats, differentiated PC12 and HAPI cells by exposing to 2% sevoflurane for 5 h. Different concentration (20, 40 and 80 µg/mL) of TAB was administrated in rats and cells. The cognitive function of rats was evaluated using the Morris water maze test and fear conditioning test. The cell proliferation and apoptosis were investigated using a CCK-8 assay and the flow cytometry. Pro-inflammatory cytokines in microglia were measured using ELISA kits. A miRNA microarray assay was conducted to screen differentially expressed miRNAs by TAB in both PC12 and HAPI cells. The luciferase reporter assay and western blot assay were used to assess the E2F1/CCNA2 and NF-κB pathways. Results TAB significantly alleviated sevoflurane-induced cognitive impairments in rats, improved PC12 cell viability, and inhibited the neuroinflammation of HAPI cells. miR-329-3p was downregulated in PC12 cells but upregulated in HAPI cells by TAB treatment, which mediated the effects of TAB on neurotoxicity and neuroinflammation. E2F1 and NF-κB P65 were two targets of miR-329-3p, and the E2F1/CCNA2 and NF-κB pathways were inhibited by miR-329-3p in PC12 and HAPI cells, respectively. Conclusions All the results provide evidence for the protective role of TAB against sevoflurane-induced cognitive impairments, which was achieved by alleviating neurotoxicity and neuroinflammation through differentially regulating miR-329-3p in neurons and microglia.

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Neuroprotection of Chikusetsu saponin V on transient focal cerebral ischemia/reperfusion and the underlying mechanism

Cited by 11 publications

References 25 publications

Influence of Melatonin on Behavioral and Neurological Function of Rats with Focal Cerebral Ischemia-Reperfusion Injury via the JNK/FoxO3a/Bim Pathway

Influence of Melatonin on Behavioral and Neurological Function of Rats with Focal Cerebral Ischemia-Reperfusion Injury via the JNK/FoxO3a/Bim Pathway

Role of traditional Chinese medicine monomers in cerebral ischemia/reperfusion injury:a review of the mechanism

Protective role of trametenolic acid B against sevoflurane-induced cognitive impairments by its different regulatory modalities of mir-329-3p in neurons and microglia

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