Catalpol ameliorates psoriasis-like phenotypes via SIRT1 mediated suppression of NF-κB and MAPKs signaling pathways

Abstract

Psoriasis is a chronic inflammatory skin disease that affects approximately 2% of worldwide population, and causing long-term troubles to the patients. Therefore, it is urgent to develop safe and effective therapeutic drugs. Catalpol is a natural iridoid glucoside, that has several remarkable pharmacological effects, however, whether catalpol can alleviated psoriasis has not been explored. The goal of the present work is to study the role of catalpol in psoriasis in vivo and in vitro. Imiquimod-induced psoriasislike mice were applied with different concentrations of catalpol for 8 consecutive days. The severity degree of psoriasis was estimated and the skin pathological changes were detected by H&E staining. Also, TNF-α-stimulated keratinocytes were treated with different concentrations of catalpol, then the oxidative stress and inflammation factors, as well as the expression of SIRT1 and activation of NF-kB and MAPK pathways were measured. The results showed that catalpol reduced the erythema, scaling, ear thickness, and changed pathological phenotypes in the lesioned skin region in mice. Treatment with catalpol significantly suppressed the oxidative stress and inflammatory reactions in vivo and in vitro, as reflected by the decreased secretion or expression of oxidative stress indicators and proinflammatory factors. Furthermore, the SIRT1 was up-regulated and the NF-κB and MAPKs signaling pathways were suppressed by the treatment of catalpol in vivo and in vitro. In summary, our data suggested that catalpol may have a therapeutic property of psoriasis by ameliorating oxidative stress and inflammation partly through SIRT1 mediated suppression of NF-κB and MAPKs pathways.

Bergamottin alleviates LPS-induced acute lung injury by inducing SIRT1 and suppressing NF-κB

“…It has been documented that SIRT1 is involved in deacetylation of NF-κB and inhibition of NF-κB activation. 21 , 22 Next, we checked whether bergamottin could promote SIRT1 expression to inhibit NF-κB signaling. LPS stimulation decreased the mRNA level of SIRT1 in the lung tissues of mice ( Figure 5C ).…”

“…SIRT1 is a protein deacetylase and has been shown to control p65 acetylation. 22 , 29 Most importantly, SIRT1 shows the capacity to alleviate LPS-induced inflammation. 30 , 31 Therefore, we speculated that bergamottin might regulate p65 activation through induction of SIRT1 and reduction of p65 acetylation.…”

Long non-coding RNA SNHG22 facilitates hepatocellular carcinoma tumorigenesis and angiogenesis via DNA methylation of microRNA miR-16-5p

“…The transfected HCC cells were seeded into 96-well plates (4 × 10 3 cells/well) and incubated for 0, 24, 48, and 72 h. Later, 10 µl of CCK8 reagent (Dojindo Laboratories) were added to incubate for another 2 h. At last, a microplate reader was used to measure the viability of cells [ 27 ].…”

Research Progress on Catalpol as Treatment for Atherosclerosis

“…SIRT1 deletion in endothelial cell (ECs), vascular smooth muscle cells (VSMCs), and monocytes/macrophages can increase OS, inflammation, foam cell formation, aging damage nitric oxide production, and autophagy and thus promote vascular aging and AS (Kitada et al, 2016). Liu et al found that catalpol inhibits NF-κB and MAPK signaling pathways by up-regulating the expression of SIRT1 mRNA and consequently reducing OS and TNF-α-induced inflammation response (Liu et al, 2021). Endogenous SIRT1 remarkably reduces endothelial activation without affecting the vasoconstriction and dilation function of ApoE−/− mice.…”