Supercritical extract of Seabuckthorn Leaves (SCE200ET) inhibited endotoxemia by reducing inflammatory cytokines and nitric oxide synthase 2 expression

Jayashankar, B.; Mishra, K.P.; Ganju, Lilly; Singh, Shashi Bala

doi:10.1016/j.intimp.2014.02.022

Cited by 24 publications

(10 citation statements)

References 27 publications

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“…These findings suggest the critical roles of iNOS/NO and COX-2/PGE 2 signaling pathways in the pathogenesis of endotoxemia. [28][29][30] Previous studies have suggested an ability of LPA to reduce the organ injury in endotoxemia and to inhibit bacterial endotoxin-induced TNF-a expression. 3,31 In fact, LPA receptors have been detected in both human and mouse macrophages, suggesting a potential role of LPA in regulating macrophage functions.…”

Section: Discussionmentioning

confidence: 99%

Attenuation of LPS-induced cyclooxygenase-2 and inducible NO synthase expression by lysophosphatidic acid in macrophages

Chien

Chuang

et al. 2015

Innate Immun

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LPS can activate the inflammatory cascades by inducing various inflammatory mediators, such as prostaglandin E(2) (PGE(2)) resulting from cyclooxygenase-2 (COX-2), and NO produced by inducible NO synthase (iNOS). Lysophosphatidic acid (LPA) has been demonstrated to participate in inflammation. This study aimed to clarify the impact and the involving mechanisms of LPA on LPS-incurred inflammation in macrophages. First, LPA appeared to attenuate LPS-induced protein and mRNA expression of COX-2 and iNOS genes, as well as production of PGE(2) and NO. By using selective inhibitors targeting various signaling players, the inhibitory G protein alpha subunit (Gα(i)) seemed to be involved in the effect of LPA; p38, ERK and NF-κB were involved in the LPS-mediated COX-2/PGE(2) pathway; and p38, JNK, phosphoinositide-3-kinase and NF-κB were involved in the LPS-mediated iNOS/NO pathway. LPA was able to diminish LPS-induced phosphorylation of p38 and Akt, as well as NF-κB p65 nuclear translocation. By utilization of inhibitors of COX-2 and iNOS, there appeared to be no modulation between the COX-2/PGE(2) and the iNOS/NO signaling pathways. Our findings demonstrate a clear anti-inflammatory role of LPA acting via Gα(i) in LPS-mediated inflammatory response in macrophages, owing, at least in part, to its suppressive effect on LPS-induced activation of p38, Akt and NF-κB.

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Section: Discussionmentioning

confidence: 99%

Attenuation of LPS-induced cyclooxygenase-2 and inducible NO synthase expression by lysophosphatidic acid in macrophages

Chien

Chuang

et al. 2015

Innate Immun

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“…Wang, et al, 2012). Furthermore, in a mouse model of LPS-induced endotoxemia, Isorhamnetin reduced peritoneal macrophages NO production, and IL-6, TNF-α, CD40, COX-2 and iNOS expression (Jayashankar, Mishra, Ganju, & Singh, 2014). These observations may indicate a correlation with TLR modulation, as induction of COX-2 and iNOS are associated with TLR4, and play pivotal roles in the development of inflammatory diseases (Shweash, et al, 2011).…”

Section: Pharmacological Approaches Targeting Tlr/nf-κb and Oxidatmentioning

confidence: 99%

Oxidative stress and cellular pathways of asthma and inflammation: Therapeutic strategies and pharmacological targets

Mishra

Banga

Silveyra

2018

Pharmacology & Therapeutics

203

127

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Asthma is a complex inflammatory disease characterized by airway inflammation and hyperresponsiveness. The mechanisms associated with the development and progression of asthma have been widely studied in multiple populations and animal models, and these have revealed involvement of various cell types and activation of intracellular signaling pathways that result in activation of inflammatory genes. Significant contributions of Toll-like-receptors (TLRs) and transcription factors such as NF-кB, have been reported as major contributors to inflammatory pathways. These have also recently been associated with mechanisms of oxidative biology. This is of important clinical significance as the observed inefficacy of current available treatments for severe asthma is widely attributed to oxidative stress. Therefore, targeting oxidizing molecules in conjunction with inflammatory mediators and transcription factors may present a novel therapeutic strategy for asthma. In this review, we summarize TLRs and NF-кB pathways in the context of exacerbation of asthma pathogenesis and oxidative biology, and we discuss the potential use of polyphenolic flavonoid compounds, known to target these pathways and possess antioxidant activity, as potential therapeutic agents for asthma.

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“…Earlier studies have also shown the SBKT to possess anti-inflammatory properties through the modulation of pro-inflammatory cytokines, cyclooxygenase-2, inducible nitric oxide synthase, and inflammasome-associated IKK-β/NF-κB pathways (Jayashankar et al, 2012; Jayashankar et al, 2014; Suchal et al, 2016; Shi et al, 2017; Tanwar et al, 2018). The anti-inflammatory property of the SBKT can be related to the presence of fatty acids, such as polyunsaturated and omega-3 fatty acid components.…”

Section: Discussionmentioning

confidence: 99%

Cytokines Driven Anti-Inflammatory and Anti-Psoriasis Like Efficacies of Nutraceutical Sea Buckthorn (Hippophae rhamnoides) Oil

et al. 2019

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Psoriasis is a chronic inflammatory skin disease characterized by circumscribed, red, thickened plaques with overlying silvery white scales. It is associated with the release of pro-inflammatory mediators that lead to the development of edema and distress. Here we show the anti-inflammatory and anti-psoriatic efficacies of a neutraceutical sea buckthorn oil (SBKT) derived from the fruit pulp of Hippophae rhamnoides. Chemical analysis of the SBKT showed the presence of 16 major saturated, mono-, and polyunsaturated fatty acids components, imparting significant nutritional values. Efficacy of the SBKT in modulating psoriasis and associated inflammation was first tested in vitro using human monocytic (THP-1) cells. SBKT induced cytotoxicity at a dose of ≥25 µl/ml. Treatment of the lipopolysaccharide-stimulated THP-1 cells with SBKT subdued the enhanced release of intracellular reactive nitrogen species and expression of NF-κB protein, in a concentration-dependent manner. This was accompanied by a reduction in the release of downstream pro-inflammatory cytokines: Interleukin-1ß and interleukin-6. Tumor necrosis factor-α released in the stimulated THP-1 cells were also inhibited by SBKT dose of 5 µl/ml. In vivo oral and topical treatment with SBKT in the Carrageenan-stimulated paw edema model, showed a significant decrease in paw volume and edema. In the 12-O tetradecanoyl phorbol 13-acetate (TPA) stimulated CD-1 mice psoriasis-like model, concurrent oral and tropical SBKT treatments substantially reduced ear edema and ear biopsy weights. Histopathologically, significant reduction in ear epidermal thickness and skin lesion scores was observed in the SBKT-treated animals. In conclusion, SBKT showed anti-inflammatory and anti-psoriasis-like efficacies in healing chemical-induced inflammation and psoriasis. The possible mode of action of SBKT was found through inhibition of reactive nitrogen species, and downregulation of NF-κB protein and pro-inflammatory cytokines. Thus, the present data suggest that Sea buckthorn oil can be used as an anti-inflammatory and anti-psoriatic nutraceutical.

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Supercritical extract of Seabuckthorn Leaves (SCE200ET) inhibited endotoxemia by reducing inflammatory cytokines and nitric oxide synthase 2 expression

Cited by 24 publications

References 27 publications

Attenuation of LPS-induced cyclooxygenase-2 and inducible NO synthase expression by lysophosphatidic acid in macrophages

Attenuation of LPS-induced cyclooxygenase-2 and inducible NO synthase expression by lysophosphatidic acid in macrophages

Oxidative stress and cellular pathways of asthma and inflammation: Therapeutic strategies and pharmacological targets

Cytokines Driven Anti-Inflammatory and Anti-Psoriasis Like Efficacies of Nutraceutical Sea Buckthorn (Hippophae rhamnoides) Oil

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