Leonurus sibiricusinduces nitric oxide and tumor necrosis factor-α in mouse peritoneal macrophages

Author:

An Hyo-Jin12345,Rim Hong-Kun12345,Lee Jong-Hyun12345,Suh Se-Eun12345,Lee Ji-Hyun12345,Kim Na-Hyung12345,Choi In-Young12345,Jeong Hyun-Ja12345,Kim Il Kwang12345,Lee Ju-Young12345,An Nyeon-Hyoung12345,Kim Hyung-Ryong12345,Um Jae-Young12345,Kim Hyung-Min12345,Hong Seung-Heon12345

Affiliation:

1. Department of Oriental Pharmacy, College of Pharmacy, Wonkwang University, Iksan, Jeonbuk 570-749, Republic of Korea.

2. College of Oriental Medicine, Kyung Hee University, Seoul, Republic of Korea.

3. Biochip Research Center, Hoseo University, Chungnam, Republic of Korea.

4. Division of Bio-Nano Chemistry, Wonkwang University, Iksan, Republic of Korea.

5. Department of Herb Science, Shinsung College, Chungnam, Republic of Korea.

Abstract

Using mouse peritoneal macrophages, we have examined the mechanism by which Leonurus sibiricus (LS) regulates nitric oxide (NO) production. When LS was used in combination with recombinant interferon-γ (rIFN-γ), there was a marked cooperative induction of NO production; however, LS by itself had no effect on NO production. The increased production of NO from rIFN-γ plus LS-stimulated cells was almost completely inhibited by pretreatment with pyrrolidine dithiocarbamate (PDTC), an inhibitor of nuclear factor κB. Furthermore, treatment of peritoneal macrophages with rIFN-γ plus LS caused a significant increase in tumor necrosis factor-α (TNF-α) production. PDTC also decreased the effect of LS on TNF-α production significantly. Because NO and TNF-α play an important role in immune function and host defense, LS treatment could modulate several aspects of host defense mechanisms as a result of stimulation of the inducible nitric oxide synthase.

Publisher

Canadian Science Publishing

Subject

Physiology (medical),Pharmacology,General Medicine,Physiology

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