Sulforaphane Suppressed LPS and Pam3CSK4 Mediated Inflammation in COPD Through MyD88-Dependent Toll-Like Receptors Pathway

Zeng, Xiaoli; Liu, Xiaoju; Bao, Hairong; Zhang, Yi; Tan, Enli

doi:10.1016/j.chest.2016.02.366

Cited by 2 publications

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“…73 Zeng et al have demonstrated that sulforaphane, an isothiocyanate naturally occurring in cruciferous vegetables, exhibits an anti-inflammatory effect by inhibiting cytokine expression via the TLR2/TLR4/MyD88 signaling pathway in macrophages derived from monocytes from patients with COPD. 74 Ma et al have shown in the experimental study that Chinese herbal granules "Bufei Yishen" are effective in reducing inflammation in COPD. The potential mechanism of their action appears to be the suppression of TLR-4/NF-κB signaling.…”

Section: Therapeutic Implications Of Tlr2 and Tlr4 Signaling Pathwaysmentioning

confidence: 99%

<p>The Role of Toll-Like Receptors 2 and 4 in the Pathogenesis of Chronic Obstructive Pulmonary Disease</p>

Sidletskaya

Виткина

Denisenko

2020

COPD

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Currently, chronic obstructive pulmonary disease (COPD) is one of the leading causes of morbidity and mortality worldwide. The determination of immune mechanisms of inflammation in the disease presents an important challenge for fundamental medical research. According to modern views, Toll-like receptors (TLRs), among which TLR2 and TLR4 play a key role, are one of the essential components of inflammatory process in COPD. This review focuses on following aspects: the role of TLR2 and TLR4 in the initiation of inflammatory process in COPD; the mechanisms of influence of various exogenous factors (cigarette smoke, suspended particulate matter, and bacteria) on the expression of TLR2 and TLR4; the contribution of these TLRs to the T-helper (Th) immune response development in COPD, in particular to the Th17 immune response, which contributes to the progression of the disease and therapeutic implications of TLR2 and TLR4 in COPD.

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Section: Therapeutic Implications Of Tlr2 and Tlr4 Signaling Pathwaysmentioning

confidence: 99%

<p>The Role of Toll-Like Receptors 2 and 4 in the Pathogenesis of Chronic Obstructive Pulmonary Disease</p>

Sidletskaya

Виткина

Denisenko

2020

COPD

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Anti-Inflammatory Therapeutic Mechanisms of Isothiocyanates: Insights from Sulforaphane

Habtemariam

2024

Biomedicines

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Isothiocyanates (ITCs) belong to a group of natural products that possess a highly reactive electrophilic -N=C=S functional group. They are stored in plants as precursor molecules, glucosinolates, which are processed by the tyrosinase enzyme upon plant tissue damage to release ITCs, along with other products. Isolated from broccoli, sulforaphane is by far the most studied antioxidant ITC, acting primarily through the induction of a transcription factor, the nuclear factor erythroid 2–related factor 2 (Nrf2), which upregulates downstream antioxidant genes/proteins. Paradoxically, sulforaphane, as a pro-oxidant compound, can also increase the levels of reactive oxygen species, a mechanism which is attributed to its anticancer effect. Beyond highlighting the common pro-oxidant and antioxidant effects of sulforaphane, the present paper was designed to assess the diverse anti-inflammatory mechanisms reported to date using a variety of in vitro and in vivo experimental models. Sulforaphane downregulates the expression of pro-inflammatory cytokines, chemokines, adhesion molecules, cycloxyhenase-2, and inducible nitric oxide synthase. The signalling pathways of nuclear factor κB, activator protein 1, sirtuins 1, silent information regulator sirtuin 1 and 3, and microRNAs are among those affected by sulforaphane. These anti-inflammatory actions are sometimes due to direct action via interaction with the sulfhydryl structural moiety of cysteine residues in enzymes/proteins. The following are among the topics discussed in this paper: paradoxical signalling pathways such as the immunosuppressant or immunostimulant mechanisms; crosstalk between the oxidative and inflammatory pathways; and effects dependent on health and disease states.

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Sulforaphane Suppressed LPS and Pam3CSK4 Mediated Inflammation in COPD Through MyD88-Dependent Toll-Like Receptors Pathway

Cited by 2 publications

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<p>The Role of Toll-Like Receptors 2 and 4 in the Pathogenesis of Chronic Obstructive Pulmonary Disease</p>

<p>The Role of Toll-Like Receptors 2 and 4 in the Pathogenesis of Chronic Obstructive Pulmonary Disease</p>

Anti-Inflammatory Therapeutic Mechanisms of Isothiocyanates: Insights from Sulforaphane

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