Active Components with Inhibitory Activities on IFN-γ/STAT1 and IL-6/STAT3 Signaling Pathways from Caulis Trachelospermi

Liu, Xiaoting; Wang, Zhexing; Yu, Yang; Wang, Lin; Sun, Ruo-Feng; Zhao, Yimin; Yu, Na

doi:10.3390/molecules190811560

Cited by 14 publications

(15 citation statements)

References 23 publications

(29 reference statements)

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“…ARC inhibited autophagy as well as apoptosis by suppressing IFN-γ/IL-6/Stat1 signaling and IL6/Bnip3 signaling. The previous study of luciferase activity test showed that ARC could inhibit the IFN-γ/Stat1 and IL-6/Stat3 signaling ( 122 ), while present study demonstrated the inhibitions of both IFN-γ/IL-6/Stat1 signaling and IL6/Bnip3 signaling contributed to the protective effects of ARC against ConA-induced hepatitis.…”

Section: Discussionsupporting

confidence: 53%

Quantitative Proteomic Analysis Reveals That Arctigenin Alleviates Concanavalin A-Induced Hepatitis Through Suppressing Immune System and Regulating Autophagy

et al. 2018

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Concanavalin A-induced autoimmune hepatitis is a well-established experimental model for immune-mediated liver injury. It has been widely used in the therapeutic studies of immune hepatitis. The in-depth analysis of dysregulated proteins from comparative proteomic results indicated that the activation of immune system resulted in the deregulation of autophagy. Follow-up studies validated that some immune related proteins, including Stat1, Pkr, Atg7, and Adrm1, were indeed upregulated. The accumulations of LC3B-II and p62 were confirmed by immunohistochemistry and Western blot analyses. Arctigenin pretreatment significantly alleviated the liver injury, as evidenced by biochemical and histopathological investigations, whose protective effects were comparable with Prednisone acetate and Cyclosporin A. Arctigenin pretreatment decreased the levels of IL-6 and IFN-γ, but increased the ones of IL-10. Next, the quantitative proteomic analysis demonstrated that ARC pretreatment suppressed the activation of immune system through the inhibition of IFN-γ signaling, when it downregulated the protein expressions of Stat1, P-Stat1, Pkr, P-Pkr, Bnip3, Beclin1, Atg7, LC3B, Adrm1, and p62. Meanwhile, Arctigenin pretreatment also reduced the gene expressions of Stat1, Pkr, and Atg7. These results suggested that Arctigenin alleviated autophagy as well as apoptosis through inhibiting IFN-γ/IL-6/Stat1 pathway and IL-6/Bnip3 pathway. In summary, the comparative proteomic analysis revealed that the activation of immune system led to Concanavalin A-induced hepatitis. Both autophagy and apoptosis had important clinical implications for the treatment of immune hepatitis. Arctigenin might exert great therapeutic potential in immune-mediated liver injury.

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Section: Discussionsupporting

confidence: 53%

Quantitative Proteomic Analysis Reveals That Arctigenin Alleviates Concanavalin A-Induced Hepatitis Through Suppressing Immune System and Regulating Autophagy

et al. 2018

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“…And it has been reported to mediate various cellular functions, including gene activation, cell differentiation, cell survival, and proliferation [18][19][20]. Notably, a number of growth factors and cytokines such as TGF-b1 [21], IFN-c [22], and IL-6 [23][24][25], oncostatin M (OSM) [26], high glucose (HG) [27], and Ang II [28] have been found to trigger this pathway, and then induce expression of multiple genes, including profibrotic [29] and pro-inflammatory genes [30]. Evidence derived from numerous clinical and animal models studies is emerging for the involvement of JAK/STAT cascade in renal disease.…”

Section: Introductionmentioning

confidence: 99%

Fluorofenidone protects against renal fibrosis by inhibiting STAT3 tyrosine phosphorylation

Tang

Liu

et al. 2015

Mol Cell Biochem

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Signaling through the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, especially JAK2/STAT3, is involved in renal fibrosis. Fluorofenidone (FD), a novel pyridone agent, exerts anti-fibrotic effects in vitro and in vivo. Herein, we sought to investigate whether FD demonstrates its inhibitory function through preventing JAK2/STAT3 pathway. In this study, we examined the effect of FD on activation of rat renal interstitial fibroblasts, glomerular mesangial cells (GMC), and expression of JAK2/STAT3. Moreover, we explored the histological protection effects of FD in UUO rats, db/db mice, and phosphorylation of JAK2/STAT3 cascade. Our studies found that pretreatment with FD resulted in blockade of activation of fibroblast and GMC manifested by fibronectin (FN) and α-smooth muscle actin (α-SMA) protein expression and decline of STAT3 tyrosine phosphorylation induced by IL-6 or high glucose. In unilateral ureteral obstruction rats and a murine model of spontaneous type 2 diabetes (db/db mice), treatment with FD blocked the expression of FN and α-SMA, prevented renal fibrosis progression, and attenuated STAT3 activation. However, FD administration did not interfere with JAK2 activation both in vivo and in vitro. In summary, the molecular mechanism by which FD exhibits renoprotective effects appears to involve the inhibition of STAT3 phosphorylation.

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“…The compound luteolin 4′- O -glucuronide [ 8 ] (7.3 mg) was obtained directly from the fraction 22. Fraction 6 was chromatographed using RP18 HPLC with MeOH/H 2 O (42:58, v/v) as mobile phase (flow rate 2.0 mL min −1 ) to yield pure compound nortrachelogenin 4,4′-di- O -ß-D-glucopyranoside ( 2 ) [ 9 ] (1.1 mg, t R 36 min). Fraction 8 was isolated using RP18 HPLC with MeOH/H 2 O (37:63, v/v) as mobile phase (flow rate 2.0 mL min −1 ) to yield pure compounds chlorogenic acid [ 10 ] (8.1 mg, t R 8 min), neochlorogenic acid [ 11 ] (3.0 mg, t R 9 min), naringenin-7- O -neohesperidoside [ 12 ] (19.2 mg, t R 27 min), quercetin-3- O - α -L-rhamnopyranosyl-(1→6)- β -D-glucopyranoside [ 13 ] (3.0 mg, t R 52 min), apigenin-7- O - α -L-rhamnopyranosyl-(1→6)- β -D-glucopyranoside [ 14 ] (1.4 mg, t R 62 min), and Kaempferol-3- O - α -L-rhamnopyranosyl-(1→6)- β -D-glucopyranoside [ 13 ] (1.9 mg, t R 82 min).…”

Section: Methodsmentioning

confidence: 99%

Antioxidant Potential of Herbal Preparations and Components from Galactites elegans (All.) Nyman ex Soldano

Tebboub

Cotugno

Oke-Altuntas

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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Galactites is a genus of flowering plants belonging to Asteraceae family. This genus is mainly represented by the Galactites elegans (All.) Nyman ex Soldano, the milky thistle, a plant of Mediterranean origin. Galactites elegans is consumed as a monofloral boar thistle honey. Chromatography separation of CHCl3 and n-BuOH extracts of aerial parts of G. elegans led to isolation of 18 pure compounds. Their structures were elucidated by 1D-and 2D-NMR spectroscopy and confirmed by mass spectrometry analysis. Sinapic aldehyde, abietin, chlorogenic acid, neochlorogenic acid, 8α-hydroxypinoresinol, 9α-hydroxypinoresinol, pinoresinol, 4-ketopinoresinol, nortrachelogenin, and erythro-guaiacylglycerol-β-O-4′-dihydroconiferyl alcohol were isolated from CHCl3 extract, while luteolin 4′-O-glucuronide, naringenin-7-O-neohesperidoside, kaempferol-3-O-α-L-rhamnopyranosyl-(1→6)-β-D-glucopyranoside, apigenin-7-O-α-L-rhamnopyranosyl-(1→6)-β-D-glucopyranoside, quercitrin, quercetin-3-O-α-L-rhamnopyranosyl-(1→6)-β-D-glucopyranoside, ciwujiatone, and nortrachelogenin-4,4′-di-O-β-D-glucopyranoside were obtained from n-BuOH extract. The majority of isolated compounds displayed a significant antioxidant potential in vitro test (DPPH). The ability of compounds to reduce the level of peroxides in control and BHP-treated Jurkat cells was studied. The lignan derivatives were also able to reduce at 50 μM the basal level of peroxides in Jurkat cells as well as counteract peroxide increase induced by BHP treatment. Particularly 8α-hydroxypinoresinol was the most active showing 70% of peroxide level inhibition.

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Active Components with Inhibitory Activities on IFN-γ/STAT1 and IL-6/STAT3 Signaling Pathways from Caulis Trachelospermi

Cited by 14 publications

References 23 publications

Quantitative Proteomic Analysis Reveals That Arctigenin Alleviates Concanavalin A-Induced Hepatitis Through Suppressing Immune System and Regulating Autophagy

Quantitative Proteomic Analysis Reveals That Arctigenin Alleviates Concanavalin A-Induced Hepatitis Through Suppressing Immune System and Regulating Autophagy

Fluorofenidone protects against renal fibrosis by inhibiting STAT3 tyrosine phosphorylation

Antioxidant Potential of Herbal Preparations and Components from Galactites elegans (All.) Nyman ex Soldano

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