potraviny/schisandra-klanospraska/schisandra-lignans

Účinky antimikrobiální

• Schisandra lignans are also

shown to have anti-viral activities, including anti-HIV activity (Chen et al., 1997; Yang etal., 2010), inhibition of HSV-2 and adenovirus (Song et al., 2013), and inhibition ofEpstein–Barr virus early antigen activation (Chen et al., 2002). The lowest EC50 valuesobtained in these studies against HIV-1 were 0.005 µg/ml for gomisin G (Chen et al., 1997)and 1.4 µg/ml for new lignans identified in the same study (Yang et al., 2010). The lowestEC50 values for HSV-2 and adenovirus were 5.85 µg/ml and 22.10 µg/ml respectively,gained with new lignans identified in the same study (Song et al., 2013). The effect ofSchisandra lignans on respiratory pathogens is not known, but Schisandra chinensis(Turcz.) Baill. is used in TCM for several indications, and one of them is treatment ofchronic cough (Chinese pharmacopoeia, 2010). In a clinical study results have suggestedthat a tincture of Schisandra fruit has alleviating effect on the symptoms of pneumonia(Pavluschenko et al., 1981, reviewed in Panossian & Wikman, 2008). In the study thecausative agent of pneumonia was not determined. Also other clinical studies made in theformer USSR with Schisandra tinctures show a reduced prevalence of influenza in studysubjects treated with Schisandra tincture (Panossian & Wikman, 2008). In addition thereare modern in vitro and in vivo studies that show Schisandra chinensis’ protecting effect inalveolar inflammation. Schisandra chinensis water extract prevented airway inflammationboth in vitro and in vivo (Bae et al., 2012).In human alveolar epithelial cells Schisandra
extracts inhibited cytokine mixture induced NO production and reduced IL-8 and MCP-1secretions. The extracts also suppressed neutrophil and macrophage infiltrations of lungtissues and increased IL-6 and TNF-?? levels in bronchoalveolar lavage fluid in LPS-treatedBALB/c mice. A pure compound, schisantherin A, was shown to alleviate acute respiratorydistress syndrome through downregulating NF-??B and MAPKs signaling pathways in vivoin a mouse model at 10 mg/kg concentration (Zhou et al., 2014).
Schisandra lignans are widely studied for their antioxidant properties, which is consideredone major mechanism responsible for the cytoprotective effects (Liu et al., 1982; Opletal etal., 2004; Guo et al., 2008; Zeng et al., 2012) (Table 2.). The antioxidant or reducingproperties of the lignans are also shown to mediate the anti-inflammatory responses. Forexample, in a study schisandrin B displayed anti-inflammatory activities which were due toalteration of cellular redox status leading to inhibition of nuclear factor (erythroid-derived2) 2 -like 2 (Nrf2) and NF-???? (Checker et al., 2012). Schisandrin B suppressed I??????degradation and nuclear translocation of NF-???? in activated lymphocytes. In the same studyschisandrin B was shown to inhibit mitogen-induced phosphorylation of c-Raf, MEK, ERK,JNK and p38. Schisandrin B-mediated activation of Nrf2 was proposed to suppress NF-????,which is a redox sensitive pathway. Nrf2 induces production of antioxidative enzymes, asNAD(P)H:quinone oxidoreductase, glutathione S-transferase, HO-1, glutathioneperoxidase, glutamate cysteine ligase, and peroxiredoxin 1. These factors are known todiminish reactive oxygen species (ROS). Thus it can be concluded that Nrf2 activation ofschisandrin B leads to anti-inflammatory responses that are mediated by ROS. It was alsonoted that schisandrin B inhibited anti-CD3/CD28 mAb-induced secretion of IL-2, IL-4,IL-6 and IFN-?? by T-cells. In two other studies schisandrin B enhanced apoptosis throughactivation of a redox-sensitive Nrf2 pathway (Chiu et al., 2009; Chiu et al., 2011). Theantioxidative activity of schisandrin B was further confirmed in a study which showedschisandrin B to inhibit the production of ROS and NADPH oxidase activity in microglia(Zeng et al., 2012). NADPH oxidase-dependent superoxide O2 and ROS formation wereLPS induced.
Immunity, inflammation, LPS-induced mechanismsSchisandra lignans are shown to be able of suppressing the inflammatory responses inducedby bacterial lipopolysaccharide, LPS (Guo et al., 2008; Oh et al., 2010) (Table 2.).Schisandrin was found to inhibit in vitro LPS-stimulated production of nitric oxide (NO),prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase(iNOS), which was shown to result from the inhibition of nuclear factor-kappaB (NF-????)reporter gene expression and activation of c-Jun N-terminal kinase JNK and p38 mitogenactivatedprotein kinases (MAPKs) (Guo et al., 2008). In another study a group of differentSchisandra lignans, Gomisin J, N and schisandrin C, were shown to reduce LPS-inducedNO production and expression of pro-inflammatory cytokines by blockage of p38 activatedMAPK, ERK1/2 and JNK phosphorylation (Oh et al., 2010). They also decreased mRNAlevels of IL-1 and IL-6 and TNF-?? in LPS-activated cells. Schisandrin C reducedphosphorylated ERK1/2 to the level of untreated control. Gomisin N did not affect p38MAPK or ERK1/2, but LPS-induced phosphorylation of JNK was reduced by gomisin Npretreatment, and also by gomisin J and schisandrin C pretreatment. One report that studiedthe anti-neuroinflammatory effects of schisandrin B showed that this schisandrin inhibitedLPS-induced neuronal cell death and LPS-induced production of NO, PGE2 and TNF-??,and downregulated expression of IL-6 and IL1beta mRNA in LPS treated microglia (Zenget al. 2012). Schisandrin B significantly reversed the LPS-induced phosphorylation ofIKK?????? and I???? and reduced the total I???? expression level in a concentration dependentmanner. Pretreatment with schisandrin B significantly decreased NO and PGE2 productionby inhibiting iNOS and COX-2 protein expression. Schisandrin B inhibited the interactionof toll-like receptor 4 (TLR4) and TLR2 with Toll adapter proteins MyD88, IRAK-1 andTRAF-6, which was proposed to indicate that schisandrin B may inhibit the IKK??????-I????-NF-???? inflammatory signaling pathway via selective antagonism of TLR4.