Schisandra (Schisandra chinensis) and Inflammation (general): evidence and sources

The present study aimed to investigate the therapeutic effects of Schisandra chinensis (SC) extract on clinical symptoms of osteoarthritis and the modulating effect on the mechanisms associated with the progression of osteoarthritis in a rat model of monosodium iodoacetate (MIA)-induced osteoarthritis. Osteoarthritis-induced rats were randomized into four groups: MIA injection control (MC), MIA injection with celecoxib (PC), MIA injection with SC extract 100 mg/kg (SC100), and MIA injection with SC extract 200 mg/kg (SC200). Another healthy group received a saline injection as a negative control (NC). During the treatment, weight-bearing measurements were performed once a week for 4 weeks. Histopathological and biochemical analyses of the joints, blood, and chondrocyte tissue were performed following the completion of treatment. Compared with MC rats, SC rats demonstrated significantly alleviated pain behavior, bone erosion, and cartilage degradation. SC reduced serum levels of matrix metalloproteinases and pro-inflammatory cytokines. SC treatment also reversed the levels of biomarkers such as Collagen II and ADAMTS4 in the cartilage tissue. Moreover, SC administration inhibited the phosphorylation levels of nuclear factor kappa B (NF-κB) and NF-κB Inhibitor alpha. This study demonstrates that SC ameliorated osteoarthritis at in vivo level. Our results suggest that SC might be a potential therapeutic agent for osteoarthritis.

Ethnopharmacological relevance Schisandra chinensis is used as a traditional Chinese medicine to treat a variety of diseases. Schisandra chinensis lignans (SCL) are one of the most active components extracted from Schisandrae chinensis fructus, exhibit a broad array of pharmacological properties, especially anti-inflammatory and hepatic lipid-lowering effects, suggesting SCL may have potential anti-nonalcoholic steatohepatitis (NASH) ability. However, the therapeutic efficacy of SCL against NASH and the underlying mechanism of this action remains unclear. Aim of the study In the current study, we aimed to investigate the anti-NASH action of SCL and explore the underlying mechanism in vitro and in vivo. We also assess the involvement of the gut-liver axis in the anti-NASH effects of SCL. Methods Palmitic acid (PA)-treated HepG2 cells, mouse primary hepatocytes (MPHs) and methionine-choline deficient (MCD) diet-fed mice were selected as NASH models. ORO staining and qRT-PCR were performed to assess hepatic steatosis and inflammatory responses, respectively. Masson's trichrome staining was used to detect the liver fibrosis. Protein expression was detected by Western blotting or immunohistochemistry. The changes of gut microbiota were analyzed using 16S rDNA sequencing in mice. The levels of metabolites in liver and feces were measured by metabolomics. Results The results showed that SCL treatment alleviated steatosis and inflammation in palmitic acid (PA)-treated HepG2 cells and mouse primary hepatocytes (MPHs). SCL treatment suppressed the phosphorylation of key components involved in NF-κB signaling and enhanced the expression of fatty acid oxidation (FAO)-related enzymes (e.g. CPT1, HMGCS2, and ACOX1) in PA-treated HepG2 cells. SCL could ameliorate hepatic steatosis and inflammation in NASH mice. SCL also ameliorated intestinal barrier injury and restructured the gut microbiota in NASH mice. SCL also modulated hepatic and colonic bile acid metabolism via FXR signaling. Conclusion These findings indicate that SCL treatment ameliorates hepatic inflammation and steatosis in NASH mice, potentially though to the suppression of NF-κB signaling and the promotion of fatty acid β-oxidation. Moreover, SCL could restore gut microbiota-mediated bile acid homeostasis via activation of FXR/FGF15 signaling. Our study presents a pharmacological rationale for using SCL in the management of NASH.

Background Schisandra chinensis (Turcz.) Baill (S. chinensis), a member of the Magnoliaceae family, is renowned for its distinctive medicinal attributes and is commonly employed in the treatment of disorders affecting the CNS. Purpose The potential therapeutic effects of a lignan-enriched extract derived from Schisandra chinensis (Turcz.) Baill (LSC) on PD is assessed, which focuses on its mechanisms of action in addressing neuroinflammation. Methods The LSC has been obtained by purifying the ethyl alcohol extract of S. chinensis. The Orbitrap-MS method has been employed to analyze the chemical composition of the LSC. In LPS-induced BV2 cells, LSC-induced changes in M1/M2 type inflammatory cytokines have been examined using the Griess reaction, Elisa, JC-1, flow cytometry, IF, and WB methods. A model of PD has been established by treatment of MPTP in C57BL/6 mice. The effect of LSC on behavioral changes, inflammatory factor levels, expression of TH and IBA-1, and production of autophagy in the midbrain has been investigated by TEM, immunohistochemistry, Elisa, and WB. Results LSC has relieved sports injuries and pathological damage, and targeted the TRPV1-AMPK-NLRP3 signaling pathway, which affected neuroinflammation and autophagy in vivo. Furthermore, in vitro investigations demonstrated that LSC has activated M1/M2 transformation, its related inflammatory factors, and protein expressions of the NLRP3-Caspase1 signaling pathway in LPS-BV2 cells. The research notably demonstrated that the LSC promoted autophagy and suppressed inflammation through targeting TRPV1. Conclusion In the investigation, LSC focused on TRPV1 and controlled neuroinflammation-autophagy by regulating AMPK-NLRP3, which has been proven for the first time. The study has presented molecular data supporting the use of LSC in treating PD and offers references for developing drugs. Remarkably, LSC has the potential to be utilized as a therapeutic or health medication that could significantly decrease PD.