Schisandrin A and B affect subventricular zone neurogenesis in mouse

Sun, Youhong; Yu, Cong; Liu, Yang; Jin, Bo; Si, Lu; Wang, Aibing; Cai, Huan; Che, Guanyu; Tang, Bo; Wang, Chunfeng; Li, Ziyi; Zhang, Xueming

doi:10.1016/j.ejphar.2014.06.032

Cited by 14 publications

(8 citation statements)

References 36 publications

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“…Schisandrin A, B, and C are the main representative lignans of S. sphenanthera , many studies focus on the connections and differences between them (Leong et al, 2016; Guo et al, 2017a,b). Although Schisandrin A and Schisandrin B share the close structure, their functions and mechanism of actions had been compared and studied in various diseases (Sun et al, 2014; Guo et al, 2017a). Previous study elucidated the protective effects of Schisandrin B on rat OA (Ran et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Schisandrin A Inhibits the IL-1β-Induced Inflammation and Cartilage Degradation via Suppression of MAPK and NF-κB Signal Pathways in Rat Chondrocytes

Huang

Xiao

et al. 2019

Front. Pharmacol.

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Osteoarthritis (OA) is a common joint disease in the elderly population. Its development has been reported to be associated with cartilage degradation and inflammatory responses. Schisandrin A, a bioactive lignin in Schisandra sphenanthera, has shown its anti-inflammatory potential in various inflammation diseases. However, the effects of Schisandrin A on OA remain to explore. In this study, rat chondrocytes were treated with IL-1β (10 ng/ml) with or without different concentrations of Schisandrin A for 24 h. Cell viability was evaluated by CCK-8 assay. Production of nitric oxide (NO) and prostaglandin E2 (PGE2) was measured by the Griess reaction and ELISA. The MAPK/NF-κB-related signaling molecules expression and the protein production of inducible nitric oxide synthase (iNOS), cyclooxygenase (Cox)-2, MMPs (MMP1, MMP3, MMP13), ADAMTS5, Collagen II, aggrecan, and Sox9 were detected by Western blot. Protein expression of Collagen II, aggrecan, and p65 nuclear translocation was evaluated by immunofluorescence. In vivo, intra-articular injection of 50 μM Schisandrin A or equal volume of vehicle was performed on rat OA models. Severity of cartilage damage was evaluated by HE and Safranin-O-Fast green staining. Our results revealed that Schisandrin A could suppress the IL-1β-induced production of NO and PGE2 in rat chondrocytes. Consistent with these findings, the upregulation of iNOS and Cox2 could also been decreased by Schisandrin A. Additionally, Schisandrin A could inhibit IL-1β-induced cartilage matrix catabolic enzymes including MMPs and ADAMTS5. Moreover, the IL-1β-induced downregulation of Collagen II, aggrecan, and Sox9 could be ameliorated by Schisandrin A. Mechanistically, Schisandrin A functioned by suppressing MAPK and NF-κB signal pathways. In vivo, Schisandrin A prevented cartilage damage in rat OA model. In conclusion, this study elucidates that Schisandrin A inhibits the IL-1β-induced inflammation and cartilage degradation via suppression of MAPK and NF-κB signal pathways, indicating its potential role in OA therapy.

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Section: Discussionmentioning

confidence: 99%

Schisandrin A Inhibits the IL-1β-Induced Inflammation and Cartilage Degradation via Suppression of MAPK and NF-κB Signal Pathways in Rat Chondrocytes

Huang

Xiao

et al. 2019

Front. Pharmacol.

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“…Schisandrin A (SchA) is a kind of active lignin from Schisandra chinensis fructus. SchA elicits a series of bioactive properties; [ 18–20 ] however, its antitumor effects have been rarely reported. As the emergence of a multidrug resistance‐reversing agent, SchA has been demonstrated to be effective in chemotherapy for doxorubicin‐resistant human osteosarcoma cells.…”

Section: Introductionmentioning

confidence: 99%

“…In addition, we emphatically conducted our study with a center of phosphatidylinositol 3 kinase/protein kinase B/nuclear factor κB (PI3K/AKT/NF‐κB) signaling cascade, which has been reported to be modulated by SchA in the studies about cell viability and metastases. [ 19,20 ]…”

Section: Introductionmentioning

confidence: 99%

MEG3 is restored by schisandrin A and represses tumor growth in choriocarcinoma cells

2020

J Biochem & Molecular Tox

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Schisandrin A (SchA) has been reported as a multidrug resistance-reversing agent; however, its antitumor effects have been rarely reported. Consequently, we attempted to explore whether SchA per se possesses an antitumor property in choriocarcinoma JEG-3 and BeWo cells and its potential mechanisms. JEG-3, BeWo, and HTR-8/SVneo cells were stimulated with SchA at different concentrations (10-100 μM), and cellular viability was evaluated with Cell Counting Kit-8. After stimulation with SchA, proliferation, apoptosis, migration, and invasion were detected by bromodeoxyuridine assay, Annexin V-fluorescein isothiocyanate/ propidium iodide (Annexin V-FITC/PI) method, and a Transwell system, in JEG-3 cells transfected with short hairpin-RNA for maternally expressed 3. Western blot was performed to quantify protein. MEG3 was examined by a quantitative reverse transcription-polymerase chain reaction. MEG3 was downregulated in choriocarcinoma tissues. SchA diminished cellular viability, decreased proliferative activity, inhibited migratory and invasive behaviors, and repressed phosphorylation of regulators of phosphatidylinositol 3 kinase/protein kinase B/nuclear factor κB (PI3K/AKT/NF-κB) signaling cascade in gestational choriocarcinoma cells. MEG3 was upregulated by SchA in JEG-3 and BeWo cells. SchA exhibited little suppressive effects in JEG-3 cells lacking MEG3. Besides, the phosphorylation of transducers was evoked in MEG3-silenced JEG-3 cells despite stimulation with SchA. SchA administration repressed the growth of JEG-3 and BeWo cells by upregulating MEG3. Besides, SchA blocked PI3K/AKT/NF-κB signal cascade by elevating MEG3. K E Y W O R D S choriocarcinoma, MEG3, PI3K/AKT/NF-κB, schisandrin A

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“…α-asarone, a bioactive compound of Acori Graminei Rhizoma, enhances proliferation and differentiation in neural progenitor cells and the DG of cultured hippocampal slices [60]. Moreover, it was reported that schisandrin, a lignan extracted from Schisandrae Fructus, enhances dendritic outgrowth and synaptogenesis in cultured hippocampal neurons [61] and schisandrin B increases neurogenesis in the subventricular zone in mice [62]. Additionally, although levels of hippocampal neurogenesis were not affected, Polygalae Radix increases mRNA expression of glial cell line-derived neurotrophic factor and dendritic spine maturation in the hippocampus and the nucleus accumbens in mice [63].…”

Section: Discussionmentioning

confidence: 99%

Jowiseungchungtang Inhibits Amyloid-β Aggregation and Amyloid-β-Mediated Pathology in 5XFAD Mice

Shin

Jeong

Jeon

et al. 2018

IJMS

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Alzheimer’s disease (AD) is a neurodegenerative disease, which is accompanied by memory loss and cognitive dysfunction. Although a number of trials to treat AD are in progress, there are no drugs available that inhibit the progression of AD. As the aggregation of amyloid-β (Aβ) peptides in the brain is considered to be the major pathology of AD, inhibition of Aβ aggregation could be an effective strategy for AD treatment. Jowiseungchungtang (JWS) is a traditional oriental herbal formulation that has been shown to improve cognitive function in patients or animal models with dementia. However, there are no reports examining the effects of JWS on Aβ aggregation. Thus, we investigated whether JWS could protect against both Aβ aggregates and Aβ-mediated pathology such as neuroinflammation, neurodegeneration, and impaired adult neurogenesis in 5 five familial Alzheimer’s disease mutations (5XFAD) mice, an animal model for AD. In an in vitro thioflavin T assay, JWS showed a remarkable anti-Aβ aggregation effect. Histochemical analysis indicated that JWS had inhibitory effects on Aβ aggregation, Aβ-induced pathologies, and improved adult hippocampal neurogenesis in vivo. Taken together, these results suggest the therapeutic possibility of JWS for AD targeting Aβ aggregation, Aβ-mediated neurodegeneration, and impaired adult hippocampal neurogenesis.

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Schisandrin A and B affect subventricular zone neurogenesis in mouse

Cited by 14 publications

References 36 publications

Schisandrin A Inhibits the IL-1β-Induced Inflammation and Cartilage Degradation via Suppression of MAPK and NF-κB Signal Pathways in Rat Chondrocytes

Schisandrin A Inhibits the IL-1β-Induced Inflammation and Cartilage Degradation via Suppression of MAPK and NF-κB Signal Pathways in Rat Chondrocytes

MEG3 is restored by schisandrin A and represses tumor growth in choriocarcinoma cells

Jowiseungchungtang Inhibits Amyloid-β Aggregation and Amyloid-β-Mediated Pathology in 5XFAD Mice

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