BACKGROUNDAlcoholic liver injury (ALI) represents a major international public health concern with no targeted pharmacological intervention and a dearth of clinical trial-approved medications for its management. The dried leaves of Schisandra chinensis (SCL) are rich in flavonoids, lignans, polysaccharides, and other active ingredients with anti-inflammatory, antioxidant, and antitumour activities and are commonly applied in the treatment of osteoarthritis, diabetes, and neurodegenerative diseases. The crude lignans of SCL have been reported to treat CCl₄-induced acute liver injury, and SCL tea has also been reported to have hepatoprotective effects. The components of SCL are currently the focus of investigation; however, conclusive pharmacological studies on SCL in the treatment of ethanol-induced ALI are rare.PURPOSEThis study aimed to identify the bioactive components and elucidate the mechanism of action of SCL against ALI.METHODSThe optimal month for harvesting SCL was first determined using a cellular ALI model. Immediately afterwards, the efficacy of SCL was evaluated based on cellular ALI model and ALI mice model. The expression levels of NLRP3 inflammasome-associated proteins were examined via Western blotting. To identify the bioactive components of SCL, the common components in 10 batches of SCL were identified by UPLC‒Q-TOF‒MS/MS. Subsequent analysis via correlation identified common elements' pharmacological impacts, filtering for substances with notable contributions to effectiveness. Finally, potential bioactive components were further identified through molecular docking and verified in ALIcell models.RESULTSSCL has the best efficacy in early August, and by improving hepatic aminotransferase activity, regulating lipid metabolism, alleviating oxidative stress, reducing the release of inflammatory mediators, and inhibiting the expression of NLRP3-related pyroptosis proteins, it plays a role in alleviating ALI. A total of 32 common components were identified in 10 batches of SCL. Through correlation analysis, 10 functional components, including Schisandrin B, Angeloylgomisin Q, Chlorogenic acid, Rutin, Schisandrin C, p-Hydroxycinnamic acid, Schisandrin A, Schisandrol A, Gomisin J, and Schisantherin B, were screened. Further screening using molecular docking identified 4 key functional components, Rutin, Chlorogenic acid, Schisandrin C, and Schisantherin B, which were verified to mitigate ethanol-induced liver damage.CONCLUSIONThe present study demonstrated that SCL prevented ALI, with the main contributing components being rutin, chlorogenic acid, pentosidine C and pentosidine B. Hence, our latest study offers significant experimental proof indicating SCL as a promising prospect for ALI prevention.

01 Jun 2025·Phytomedicine

Schisandrin B regulates mitochondrial dynamics via AKT1 activation and mitochondrial targeting to ameliorate renal ischemia-reperfusion injury

Article

Author: Deng, Yun ; Yang, Li ; Li, Yi ; Wang, Hailong ; Man, Jiangwei ; Cheng, Kun ; Gui, Huiming ; Niu, Jiping ; Xu, Changhong ; Fu, Shengjun ; Wang, HuaBin

BACKGROUNDRenal ischemia-reperfusion injury (RIRI) is a significant cause of acute kidney injury(AKI) and delayed graft function(DGF), impacting post-transplant outcomes. Mitochondrial dynamics, in particular fission and fusion, play a pivotal role in the cellular response to RIRI. The modulation of these dynamics represents a potential therapeutic target. Schisandrin B (Sch B), a component derived from traditional Chinese medicine, has shown protective roles in various organ injuries, but its effect on RIRI through mitochondrial dynamics remains unexplored.OBJECTIVEThis study explores the previously uninvestigated role of Sch B in modulating mitochondrial dynamics as a potential means of alleviating RIRI. By focusing on mitochondrial fission and fusion, this research provides novel insights into the therapeutic potential of Sch B, distinguishing it from existing approaches.METHODSHK-2 cells were treated with hypoxia/reoxygenation (HR) in order to simulate renal ischemia-reperfusion injury (RIRI) in vitro. In vivo, mice underwent renal ischemia followed by reperfusion, which allowed for the simulation of the injury. Sch B's impact on mitochondrial dynamics, apoptosis, and oxidative stress was assessed through mitochondrial morphology assays, Western blotting for mitochondrial and apoptotic markers, TUNEL staining, and measurement of reactive oxygen species. Key molecular interactions were explored via Western blotting, molecular docking, SPR, and cellular thermal shift assays. In vivo, renal pathological damage was evaluated using HE, PAS, and TUNEL staining, while immunohistochemistry and immunofluorescence were employed to detect the expression levels of mitochondrial dynamics proteins and p-AKT1.RESULTSFirst, we unveiled that Schisandrin B (Sch B) significantly mitigated oxidative stress and apoptosis in HK-2 cells subjected to hypoxia-reoxygenation conditions. Sch B pretreatment notably enhanced cell viability and mitochondrial function, demonstrating its superior antioxidant capabilities compared to NAC. Second, we discovered that Sch B's protective effects involve regulating mitochondrial dynamics by decreasing fission markers, such as DRP1, while increasing fusion proteins, including OPA1 and MFN2. Furthermore, our studies revealed that Sch B directly binds to AKT1, promoting its phosphorylation and localization to mitochondria, thereby enhancing mitochondrial resilience. Finally, we demonstrated that in vivo administration of Sch B reduced renal damage and apoptosis in mouse models of renal ischemia-reperfusion injury (RIRI), while immunohistochemical analyses unveiled its role in promoting mitochondrial fusion and reducing fission, marking a significant advancement in understanding Sch B's therapeutic potential in RIRI.CONCLUSIONOur findings demonstrate for the first time that Sch B directly interacts with AKT1 protein, enhancing its phosphorylation and promoting mitochondrial localization. This innovative mechanism reduces oxidative stress, apoptosis, and mitochondrial fission, highlighting Sch B's unique capability to modulate mitochondrial dynamics in RIRI. These results establish Sch B as a promising therapeutic agent, offering a new dimension in the management of RIRI by targeting mitochondrial health.

01 May 2025·Naunyn-Schmiedeberg's Archives of Pharmacology

Identification of potential mechanisms of Schisandrin B in the treatment of idiopathic pulmonary fibrosis by integrating network pharmacology and experimental validation

Article

Author: Zhu, Dongwei ; Li, Tingyuan ; Pan, Tingyu ; Feng, Fanchao ; Wang, Zhichao ; Qiu, Xirui ; Zhou, Xianmei ; Xu, Yong ; Wang, Jing ; Wu, Jieyu

Idiopathic pulmonary fibrosis (IPF) is a worsening fibrotic condition characterized by a short survival rate and limited treatment options. This study evaluates the potential anti-fibrotic properties of Schisandrin B (Sch B) through network pharmacology and experimental validation. A mouse model of bleomycin-induced pulmonary fibrosis was established, and the modeled mice were treated with Sch B at three doses (20 mg/kg/day, 40 mg/kg/day, and 80 mg/kg/day). A fibrotic model was developed in NIH/3T3 cells by treating them with TGF-β (10 ng/mL) and administering Sch B at various concentrations (10, 20, and 40 µM). The results revealed that Sch B treatment delayed the development of bleomycin-induced pulmonary fibrosis and substantially decreased the transcription levels of collagen I and α-SMA in TGF-β-induced fibroblasts. Core targets were screened with protein-protein interaction network analysis, molecular complex detection (MCODE), and CytoHubba plugin. The application of Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and molecular docking highlighted the significance of the HIF-1α signaling pathway in the potential mechanism of Sch B in IPF therapy. Western blot, PCR, and immunofluorescence were performed to validate the effects of Sch B on HIF-1α. In vivo and in vitro, Sch B administration reduced HIF-1α expression. These outcomes provide valuable insights into the potential mechanism by which Sch B delays IPF development, with HIF-1α potentially serving as a key target. However, further investigation is warranted to assess the safety and efficacy of Sch B in clinical settings.

100 Deals associated with Schisandrin B

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Indication	Highest Phase	Country/Location	Organization	Date
Alzheimer Disease	Phase 1	United States	-	-
Reperfusion Injury	Phase 1	United States	-	-

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