Use of herbal preparations in the treatment of oxidant-mediated inflammatory disorders

Kaplan, Mitchell; Mutlu, Ece; Benson, Mark D.; Fields, Jeremy Z.; Banan, Ali; Keshavarzian, Ali

doi:10.1016/j.ctim.2006.06.005

Cited by 84 publications

(60 citation statements)

References 82 publications

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confidence: 99%

“…In macrophages, lipopolysaccharide (LPS), a major component of bacterial cell walls, potently increases the levels of cellular reactive oxygen species (ROS) and MAPK phosphorylation, resulting in promoting proinflammatory responses (51). Consistently, specific inhibition of cellular ROS and MAPK suppresses inflammatory signaling, implying that the cellular regulator for ROS and MAPK activity might be a key factor for inflammatory responses (25,48).Berberine (BBR) is a major form of isoquinoline alkaloid derived from medicinal herbs such as Hydrastis canadensis (goldenseal), Cortex phellodendri (huangbai), and Rhizoma coptidis (huanglian), showing antibacterial and antipyretic activities (40). Recent studies have demonstrated that the beneficial effects of BBR on metabolic disorders including weightreducing, cholesterol-lowering, anti-lipogenic, and hypoglycemic effects (23,28,33,54) are associated with activation of AMP-activated protein kinase (AMPK) in peripheral tissues (3,7,33).…”

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Berberine suppresses proinflammatory responses through AMPK activation in macrophages

Jeong

Hsu²,

Lee³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

391

306

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Jeong HW, Hsu KC, Lee J-W, Ham M, Huh JY, Shin HJ, Kim WS, Kim JB. Berberine suppresses proinflammatory responses through AMPK activation in macrophages. Am J Physiol Endocrinol Metab 296: E955-E964, 2009. First published February 10, 2009 doi:10.1152/ajpendo.90599.2008 has been shown to improve several metabolic disorders, such as obesity, type 2 diabetes, and dyslipidemia, by stimulating AMP-activated protein kinase (AMPK). However, the effects of BBR on proinflammatory responses in macrophages are poorly understood. Here we show that BBR represses proinflammatory responses through AMPK activation in macrophages. In adipose tissue of obese db/db mice, BBR treatment significantly downregulated the expression of proinflammatory genes such as TNF-␣, IL-1␤, IL-6, monocyte chemoattractant protein-1 (MCP-1), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). Consistently, BBR inhibited LPS-induced expression of proinflammatory genes including IL-1␤, IL-6, iNOS, MCP-1, COX-2, and matrix metalloprotease-9 in peritoneal macrophages and RAW 264.7 cells. Upon various proinflammatory signals including LPS, free fatty acids, and hydrogen peroxide, BBR suppressed the phosphorylation of MAPKs, such as p38, ERK, and JNK, and the level of reactive oxygen species in macrophages. Moreover, these inhibitory effects of BBR on proinflammatory responses were abolished by AMPK inhibition via either compound C, an AMPK inhibitor, or dominant-negative AMPK, implying that BBR would downregulate proinflammatory responses in macrophages via AMPK stimulation.mitogen-activated protein kinase; adenosine 5Ј-monophosphate-activated protein kinase; reactive oxygen species INFLAMMATION IS AN IMPORTANT RESPONSE that protects host organisms against external injuries and pathogens. Nevertheless, many recent reports (19,42,49) have suggested that obesity is tightly associated with a chronic and low-grade inflammatory state. In obese subjects, macrophage infiltration is increased into the adipose tissue, which contributes to developing insulin resistance (16,43). Inflammation is also known to trigger atherosclerosis, a coronary artery disease the hallmark of which is the formation of fatty deposits inside the artery walls (17,35,36). Thus accumulating evidence suggests that chronic inflammatory processes would constitute a crucial part in the pathogenesis of metabolic disorders including obesity, lipid dysregulation, insulin resistance, and atherosclerosis.Cellular events of inflammatory responses are associated with the redox balance and mitogen-activated protein kinase (MAPK) signaling pathways. In macrophages, lipopolysaccharide (LPS), a major component of bacterial cell walls, potently increases the levels of cellular reactive oxygen species (ROS) and MAPK phosphorylation, resulting in promoting proinflammatory responses (51). Consistently, specific inhibition of cellular ROS and MAPK suppresses inflammatory signaling, implying that the cellular regulator for ROS and MAPK activity might be a key factor for inflammatory respons...

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confidence: 99%

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confidence: 99%

Berberine suppresses proinflammatory responses through AMPK activation in macrophages

Jeong

Hsu²,

Lee³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

391

306

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“…The oxidative modifications in the intracellular and/or cellular membrane have been defined as the result of the imbalance between ROS production and the defense mechanisms. Such alterations can lead to a high number of diseases including diabetes, cancers and cardiovascular diseases [9]. Furthermore, an increase in ROS can also cause lipids peroxidation in food during the manufacturing and storage process.…”

Section: Introductionmentioning

confidence: 99%

Phenolic extracts of Centaurium erythraea with novel antiradical, antibacterial and antileishmanial activities

Bouyahya¹,

Bakri²,

Belmehdi³

et al. 2017

APJTD

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“…The situation might be partly due to the relatively weak antioxidative property of alkaloids, because reactive oxygen species and NO (a radical) are involved in the inflammatory process. 6) We decided to investigate fourteen alkaloids from herbal plants ( Fig. 1) for their effect on TNF-a and NO production.…”

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Inhibitory Effects of Herbal Alkaloids on the Tumor Necrosis Factor-.ALPHA. and Nitric Oxide Production in Lipopolysaccharide-Stimulated RAW264 Macrophages

Yamazaki

Kawano

2011

Chem. Pharm. Bull.

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Uncontrolled production of proinflammatory cytokines is the primary cause of chronic inflammatory diseases such as rheumatoid arthritis, psoriasis, and ulcerative colitis. 1)Among the above cytokines, tumor necrosis factor-a (TNFa) plays important multiple roles in the pathobiology of inflammation, and induces itself as well as other inflammatory cytokines. Nitric oxide (NO) is another potent proinflammatory mediator. NO at low concentrations is the essential regulator of physiological homeostasis in cardiovascular system, but its overproduction by inducible nitric oxide synthase (iNOS) in the inflammation exerts harmful effects on the bodies.2) Although many synthetic drugs and biologics have been developed for suppressing TNF-a 3) and NO, 2) application of natural products of the same activity in dietary plants without or with other functional food factors like polyunsaturated fatty acids 4) is an attractive alternative, especially for ameliorating long-lasting inflammatory condition. The benefit of this approach is a better quality of life for the patients and reduction of medical costs.The anti-inflammatories, that is, TNF-a suppressing phytochemicals so far reported are mainly phenolic compounds with antioxidative property (e.g., flavonoids and stilbenoids). 5)Another major class of natural products, alkaloids, has received little attention in this regard. The situation might be partly due to the relatively weak antioxidative property of alkaloids, because reactive oxygen species and NO (a radical) are involved in the inflammatory process. 6)We decided to investigate fourteen alkaloids from herbal plants (Fig. 1) for their effect on TNF-a and NO production. Five b-carboline alkaloids (1-5), four indole alkaloids (6-9) and three quinoline alkaloids (10-12) were arbitrarily chosen from textbooks of pharmacognosy 7) and catalogues of commercial reagents, and two Lycoris alkaloids (13, 14) were included to confirm the previous report on their anti-TNF-a activity.8) These compounds are known to have various pharmacological activities (e.g., monoamine oxidase inhibition for 3-5, 9) intellectual capacity improvement for 7, anti- It is beneficial to treat chronic inflammatory condition in patients through diets that inhibit the production of proinflammatory cytokines and mediators such as tumor necrosis factor-a a (TNF-a a) and nitric oxide (NO). Since less attention has been paid to alkaloids in the diets than to polyphenols in this regard, we aimed at investigating anti-inflammatory activity of herb-derived alkaloids through suppression of TNF-a a and NO production in lipopolysaccharide (LPS)-stimulated mouse RAW264 and/or human THP-1 cells. A harmala alkaloid, harmine, an opium alkaloid, papaverine, and Lycoris alkaloids, lycorine and lycoricidinol, showed TNF-a a suppressive activities stronger than or comparable to that of a reference polyphenol, butein, in RAW264 cells (IC 50 ‫؍‬ ‫,4؍‬ 10, 2.1, 0.02, and 8 m mM, respectively). Other alkaloids showed no or marginal to moderate inhibitory activities. Similar te...

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Use of herbal preparations in the treatment of oxidant-mediated inflammatory disorders

Cited by 84 publications

References 82 publications

Berberine suppresses proinflammatory responses through AMPK activation in macrophages

Berberine suppresses proinflammatory responses through AMPK activation in macrophages

Phenolic extracts of Centaurium erythraea with novel antiradical, antibacterial and antileishmanial activities

Inhibitory Effects of Herbal Alkaloids on the Tumor Necrosis Factor-.ALPHA. and Nitric Oxide Production in Lipopolysaccharide-Stimulated RAW264 Macrophages

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