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Toxins 2017, 9(9), 275; doi:10.3390/toxins9090275

Typhonium giganteum Lectin Exerts A Pro-Inflammatory Effect on RAW 264.7 via ROS and The NF-κB Signaling Pathway

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School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China
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Jiangsu Key Laboratory of Chinese Medicine Processing, Nanjing University of Chinese Medicine, Nanjing 210023, China
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Engineering Center of State Ministry of Education for Standardization of Chinese Medicine Processing, Nanjing 210023, China
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State Key Laboratory Cultivation Base for TCM Quality and Efficacy, Nanjing University of Chinese Medicine, Nanjing 210023, China
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Yancheng Traditional Chinese Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Yancheng 224000, China
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Authors to whom correspondence should be addressed.
Academic Editor: Tomas Girbes
Received: 8 August 2017 / Revised: 4 September 2017 / Accepted: 5 September 2017 / Published: 7 September 2017
(This article belongs to the Section Plant Toxins)
View Full-Text   |   Download PDF [4087 KB, uploaded 7 September 2017]   |  

Abstract

Typhonii rhizoma, a widely used herb in traditional Chinese medicine, has acute irritating toxicity related to Typhonium giganteum lectin (TGL). TGL exhibits acute inflammatory effects, but the underlying molecular mechanisms are largely unknown. This paper is designed to assess the pro-inflammatory response of TGL on RAW 264.7 cells. RAW 264.7 treated with 6.25, 12.5, 25, and 50 µg/mL TGL showed elevated levels of inflammatory factors (TNF-α, IL-1β) and of p-IκB and p-p65, all dose-dependent, indicating that TGL had a substantial inflammatory effect and mobilized the nuclear factor-κB (NF-κB) pathway. All four TGL treatments also induced the up-regulation of reactive oxygen species (ROS) and cytosolic free Ca2+ and down-regulation of mitochondrial membrane potential (MMP). The production of cytokines and p-IκB, p-p65 were reduced by N-acetylcysteine (NAC), an ROS scavenger, which somewhat abrogated ROS production. The results showed the TGL-activated inflammatory signaling pathway NF-κB to be associated with the overproduction of ROS. Moreover, 50 μg/mL treatment with TGL led to cell apoptosis after 1 h and increased necrosis over time. These results provided potential molecular mechanisms for the observed inflammatory response to TGL including up-regulation of ROS and cytosolic free Ca2+, down-regulation of MMP, the mobilization of the NF-κB pathway, and the subsequent overproduction of pro-inflammatory factors resulting in apoptosis. Long-term stimulation with TGL resulted in strong toxic effects related to inflammation that induced necrosis in macrophages. View Full-Text
Keywords: Typhonium giganteum lectin; inflammation; oxidative stress; ROS; NF-κB; apoptosis; necrosis; Bai Fu Zi Typhonium giganteum lectin; inflammation; oxidative stress; ROS; NF-κB; apoptosis; necrosis; Bai Fu Zi
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Wang, W.; Wu, H.; Yu, H.; Zhang, X.; Cui, G.; Wang, K.; Mao, S.; Pan, Y. Typhonium giganteum Lectin Exerts A Pro-Inflammatory Effect on RAW 264.7 via ROS and The NF-κB Signaling Pathway. Toxins 2017, 9, 275.

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