Oridonin's therapeutic effect: Suppressing <scp>T</scp>h1/<scp>T</scp>h17 simultaneously in a mouse model of <scp>C</scp>rohn's disease

Wang, Shubei; Zhang, Yong; Saas, Philippe; Wang, Haili; Xü, Ying; Chen, Ke; Zhong, Jie; Yuan, Yaozong; Wang, Ying; Sun, Yifeng

doi:10.1111/jgh.12710

Cited by 43 publications

(29 citation statements)

References 35 publications

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“…Moreover, oridonin pretreatment inhibits the release of pro-inflammatory mediators, including nitric oxide, TNF alpha, IL-1 beta, and IL-6, resulting in the inhibition of the DNA-binding activity of NF-kappa B [ 45 ]. Oridonin is also reported to be a potential modulator for trinitrobenzene sulfonic acid-induced colitis and other Th1/Th17-mediated inflammatory diseases [ 108 ].…”

Section: Immunomodulatory Effectsmentioning

confidence: 99%

Molecular Insight in the Multifunctional Effects of Oridonin

Owona

Schluesener

2015

Drugs R D

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Oridonin has attracted considerable attention in the last decade because of its anti-cancer pharmacological properties. This ent-kaurane diterpenoid, isolated from the Chinese herb Rabdosia rubescens and some related species, has demonstrated great potential in the treatment profile of many diseases by exerting anti-tumor, anti-inflammatory, pro-apoptotic, and neurological effects. Unfortunately, the mechanisms via which oridonin exerts these effects remain poorly understood. This review provides an overview of the multifunctional effects of oridonin as well as the reasons for its potential for investigations in the treatment of many diseases other than cancer.

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Section: Immunomodulatory Effectsmentioning

confidence: 99%

Molecular Insight in the Multifunctional Effects of Oridonin

Owona

Schluesener

2015

Drugs R D

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“…Th1 cells, the chief mediators in type 1 immunity, can secrete interferon-γ (IFN-γ) (the iconic product of Th1 cells), interleukin 12 (IL-12), and tumor necrosis factor-α (TNF-α) which, in turn, induce TNF-α, IL-6, and IL-1β to release from macrophages. Wang et al have found that the clinical course of CD-like mouse colitis has been improved by inhibiting the activation of Th1/Th17 cells [ 15 ]. The activated Th2 cells and the cytokines secreted by Th2 cells, such as IL-4, IL-5, IL-9, IL-10, IL-23, and IL-25, have increased in inflamed mucosa of UC patients than in CD ones [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Catechins and Their Therapeutic Benefits to Inflammatory Bowel Disease

2017

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Catechins are natural polyphenolic phytochemicals that exist in food and medicinal plants, such as tea, legume and rubiaceae. An increasing number of studies have associated the intake of catechins-rich foods with the prevention and treatment of chronic diseases in humans, such as inflammatory bowel disease (IBD). Some studies have demonstrated that catechins could significantly inhibit the excessive oxidative stress through direct or indirect antioxidant effects and promote the activation of the antioxidative substances such as glutathione peroxidases (GPO) and glutathione (GSH), reducing the oxidative damages to the colon. In addition, catechins can also regulate the infiltration and proliferation of immune related-cells, such as neutrophils, colonic epithelial cells, macrophages, and T lymphocytes, helping reduce the inflammatory relations and provide benefits to IBD. Perhaps catechins can further inhibit the deterioration of intestinal lesions through regulating the cell gap junctions. Furthermore, catechins can exert their significant anti-inflammatory properties by regulating the activation or deactivation of inflammation-related oxidative stress-related cell signaling pathways, such as nuclear factor-kappa B (NF-κB), mitogen activated protein kinases (MAPKs), transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2), signal transducer and the activator of transcription 1/3 (STAT1/3) pathways. Finally, catechins can also stabilize the structure of the gastrointestinal micro-ecological environment via promoting the proliferation of beneficial intestinal bacteria and regulating the balance of intestinal flora, so as to relieve the IBD. Furthermore, catechins may regulate the tight junctions (TJ) in the epithelium. This paper elaborates the currently known possible molecular mechanisms of catechins in favor of IBD.

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“…Oridonin, an ent-kaurane diterpenoid isolated from Rabdosia rubescens (Donglingcao), has various pharmacological and biological properties such as anti-inflammatory, antiviral, and antibacterial activities [8]. Many studies have suggested that oridonin has potent anticancer activity against several cancers, including lung cancer, colorectal cancer, and hepatocellular carcinoma, in vitro and in vivo [9][10][11][12] and may exert beneficial effect against Alzheimer's disease [13], acute lung injury [14], postinflammatory irritable bowel syndrome [15], and Crohn's disease [16]. ese diseases are closely related to inflammation.…”

Section: Introductionmentioning

confidence: 99%

Oridonin Attenuates Lipopolysaccharide‐Induced ROS Accumulation and Inflammation in HK‐2 Cells

Huang

Cui

Hsu

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Renal tubulointerstitial inflammation plays an important role in chronic kidney disease (CKD). Inflammation reduction is a good strategy to combat CKD. Oridonin, an ent-kaurane diterpenoid isolated from Rabdosia rubescens (Donglingcao), is considered as an effective natural candidate for the treatment of anti-inflammatory, antiviral, and antibacterial activities, including liver fibrosis and many tumors; however, no study has demonstrated its effect on lipopolysaccharide- (LPS-) induced renal inflammation. To investigate the anti-inflammatory effects of oridonin on human renal proximal tubular epithelial cells (HK-2 cells), the expression levels of c-Jun N-terminal kinase (JNK) and reactive oxygen species (ROS) were evaluated by Western blot analysis and 2′,7′-dichlorofluorescein diacetate (DCF-DA) staining, respectively. The level of intracellular ROS increased in a dose-dependent manner following LPS treatment, whereas oridonin inhibited this effect, suggestive of its ability to prevent ROS accumulation. As the mitogen-activated protein kinase (MAPK) family of enzymes plays an important role in physiological responses, we examined the activation of JNK by Western blotting and found that oridonin attenuated LPS-induced JNK phosphorylation. Oridonin also attenuated RAW 264.7 cell chemotaxis towards LPS-treated HK-2 cells. Taken together, oridonin protected against LPS-induced inflammation including ROS accumulation, JNK activation, NF-κB nuclear translocation in HK-2 cells, and functionally blocked macrophage chemotaxis towards LPS-treated HK-2 cells. Oridonin may exhibit therapeutic potential by the anti-inflammation effect in LPS-treated HK-2 cells.

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Oridonin's therapeutic effect: Suppressing Th1/Th17 simultaneously in a mouse model of Crohn's disease

Abstract: Oridonin is a potential modulator for trinitrobenzene sulfonic acid-induced colitis and other Th1/Th17 mediated inflammatory diseases.

Cited by 43 publications

References 35 publications

Molecular Insight in the Multifunctional Effects of Oridonin

Molecular Insight in the Multifunctional Effects of Oridonin

Catechins and Their Therapeutic Benefits to Inflammatory Bowel Disease

Oridonin Attenuates Lipopolysaccharide‐Induced ROS Accumulation and Inflammation in HK‐2 Cells

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