Andrographolide sulfonate ameliorates experimental colitis in mice by inhibiting Th1/Th17 response

Liu, Wen; Guo, Wenjie; Guo, Lu; Gu, Yanhong; Cai, Peifen; Xie, Ning; Yang, Xiaoling; Shu, Yongqian; Wu, Xuefeng; Sun, Yang; Xu, Qiang

doi:10.1016/j.intimp.2014.03.015

Cited by 67 publications

(42 citation statements)

References 34 publications

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“…Bcl-2 is capable of forming a heterodimer with Bax, thereby preventing Bax homodimerization and the sequential activation of Caspase-3 [37]. NF-κB controls the expression of genes involved in a number of physiological responses including immune inflammatory responses, acute-phase inflammatory responses, oxidative stress responses, cell adhesion, differentiation, and apoptosis [38]. Through blocking the NF-κB pathway, PLD may simultaneously suppress the inflammatory activity and apoptosis activity in LPS or BLE-induced ALI.…”

Section: Discussionmentioning

confidence: 99%

Platycodin D attenuates acute lung injury by suppressing apoptosis and inflammation in vivo and in vitro

Tao

Wang

et al. 2015

International Immunopharmacology

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Section: Discussionmentioning

confidence: 99%

Platycodin D attenuates acute lung injury by suppressing apoptosis and inflammation in vivo and in vitro

Tao

Wang

et al. 2015

International Immunopharmacology

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“…The combination of andrographolide and radiation therapy can enhance the levels of apoptosis and autophagy in nude mice xenografted by human ovarian cancer skov3 (149). It was reported that andrographolide sulfonate could inhibit the p38 mitogen-activated protein kinase (p38 MAPK) and NF-κB signaling pathways, which contributed to the reduction of pro-inflammatory cytokines production in trinitrobenzene sulfonic acid (TNBS)-induced colitis mice model and further intervened the progression of colitis (150). In addition, Guo et al (151) demonstrated that andrographolide could enhance mitophagy in macrophages, lead to the reverse of mitochondrial membrane potential, and thus alleviate the symptoms of DSS-induced colitis through the inhibition of NLRP3 inflammasome activity.…”

Section: Pharmacological Intervention Of Autophagy In the Treatment Omentioning

confidence: 99%

Intestinal Autophagy and Its Pharmacological Control in Inflammatory Bowel Disease

Peng

Shao

et al. 2017

Front. Immunol.

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Intestinal mucosal barrier, mainly composed of the intestinal mucus layer and the epithelium, plays a critical role in nutrient absorption as well as protection from pathogenic microorganisms. It is widely acknowledged that the damage of intestinal mucosal barrier or the disturbance of microorganism balance in the intestinal tract contributes greatly to the pathogenesis and progression of inflammatory bowel disease (IBD), which mainly includes Crohn’s disease and ulcerative colitis. Autophagy is an evolutionarily conserved catabolic process that involves degradation of protein aggregates and damaged organelles for recycling. The roles of autophagy in the pathogenesis and progression of IBD have been increasingly studied. This present review mainly describes the roles of autophagy of Paneth cells, macrophages, and goblet cells in IBD, and finally, several potential therapeutic strategies for IBD taking advantage of autophagy.

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“…16 Another report indicated that because of its TNF-α, interleukin (IL)-1β, and nuclear factor-κB inhibitory activities, AG has been utilized extensively for the treatment of IBD. 17,18 However, the oral bioavailability of AG is low because of its low aqueous solubility (0.07 mg/mL in water) and low oral absorption due to rapid and extensive metabolism and efflux by P-glycoprotein (P-gp) in the intestine. 19,20 Thus, to overcome the problem of low oral bioavailability, improvements to the solubility of AG and prevention of its efflux by P-gp are urgently required.…”

Section: Introductionmentioning

confidence: 99%

Nanoemulsion as a strategy for improving the oral bioavailability and anti-inflammatory activity of andrographolide

Yen

Chen

et al. 2018

IJN

104

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Background Andrographolide (AG), a compound with low water solubility, possesses various pharmacological activities, particularly anti-inflammatory activity. However, its low oral bioavailability is a major obstacle to its potential use. This study developed and optimized an AG-loaded nanoemulsion (AG-NE) formulation to improve AG oral bioavailability and its protective effects against inflammatory bowel disease. Methods A high-pressure homogenization technique was used to prepare the AG-NE and solubility, viscosity, and droplet size tests were conducted to develop the optimized AG-NE composed of α-tocopherol, ethanol, Cremophor EL, and water. The permeability was assessed using everted rat gut sac method and in vivo absorption and anti-inflammatory effect in rats was also evaluated. The plasma concentration of AG was determined using our validated high performance liquid chromatography method, which was used to generate a linear calibration curve over the concentration range of 0.1–25 μg/mL in rat plasma ( R 2 >0.999). Results The optimized AG-NE had a droplet size of 122±11 nm confirmed using transmission electron microscopy and a viscosity of 28 centipoise (cps). It was stable at 4 and 25°C for 90 days. An ex vitro intestinal permeability study indicated that the jejunum was the optimal site for AG absorption from the optimized AG-NE, which was 8.21 and 1.40 times higher than that from an AG suspension and AG ethanol solution, respectively. The pharmacokinetic results indicate that the absorption of AG from AG-NE was significantly enhanced in comparison with that from the AG suspension, with a relative bioavailability of 594.3%. Moreover, the ulcer index and histological damage score of mice with indomethacin-induced intestinal lesions were significantly reduced by AG-NE pretreatment. Conclusion We conclude that the developed AG-NE not only enhanced the oral bioavailability of AG in this study but may also prove to be an effective formulation of AG for preventing gastrointestinal inflammatory disorders.

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Andrographolide sulfonate ameliorates experimental colitis in mice by inhibiting Th1/Th17 response

Cited by 67 publications

References 34 publications

Platycodin D attenuates acute lung injury by suppressing apoptosis and inflammation in vivo and in vitro

Platycodin D attenuates acute lung injury by suppressing apoptosis and inflammation in vivo and in vitro

Intestinal Autophagy and Its Pharmacological Control in Inflammatory Bowel Disease

Nanoemulsion as a strategy for improving the oral bioavailability and anti-inflammatory activity of andrographolide

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