Inflammatory and Apoptotic Regulatory Activity of Tanshinone IIA in Helicobacter pylori-Infected Cells

• Published in: The American journal of Chinese medicine (1979) Vol. 44; no. 6; p. 1187
• Main Authors: Chen, Guan-Yu, Shu, Yu-Chieh, Chuang, Duen-Yau, Wang, Yuan-Chuen
• Format: Journal Article
• Language: English
• Published: Singapore 01.01.2016
• Subjects: Animals; Apoptosis - drug effects; Apoptosis - genetics; bcl-2-Associated X Protein - genetics; bcl-2-Associated X Protein - metabolism; Caspase 9 - genetics; Caspase 9 - metabolism; Cell Line, Tumor; Diterpenes, Abietane - isolation & purification; Diterpenes, Abietane - pharmacology; Diterpenes, Abietane - therapeutic use; Gene Expression - drug effects; Gene Expression - genetics; Helicobacter pylori - pathogenicity; Humans; Inflammation - drug therapy; Inflammation - genetics; Inflammation - microbiology; Inflammation Mediators - metabolism; Mice; Mitogen-Activated Protein Kinases - genetics; Mitogen-Activated Protein Kinases - metabolism; NF-kappa B - genetics; NF-kappa B - metabolism; Phytotherapy; RAW 264.7 Cells; Salvia miltiorrhiza - chemistry; Signal Transduction - genetics; Signal Transduction - physiology; Stomach Neoplasms - prevention & control; Tanshinone IIA; Inflammation; Regulation; Helicobacter pylori; Apoptosis
• DOI: 10.1142/S0192415X1650066X
• ISSN: 0192-415X

Helicobacter pylori infections induce host cell inflammation and apoptosis, however, they are conflicting. Tanshinone IIA is an active compound of Salvia miltiorrhiza Bge. In this study, we investigated the regulatory effects of tanshinone IIA on H. pylori-induced inflammation and apoptosis in vitro. Tanshinone IIA treatments (13.6-54.4[Formula: see text][Formula: see text]M) significantly decreased nuclear factor kappa B (NF-kB) and mitogen-activated protein kinase (MAPK) [p-38 and C-terminal Jun-kinase 1/2 (JNK1/2)] protein expressions and inflammatory substance [cyclooxygenase-2 (COX-2), 5-lipooxygenase (5-LOX), intercellular adhesion molecule-1 (ICAM-1), reactive oxygen species (ROS), nitric oxide (NO), inducible nitric oxide synthase (iNOS), interleukin-1[Formula: see text] (IL-1[Formula: see text], IL-6, and IL-8] production in the H. pylori-infected cells. In contrast, tanshinone IIA treatments significantly increased apoptotic relevant protein [Bcl-2-associated X protein (Bax) and caspase 9] expressions and increased mitochondrial transmembrane potential ([Formula: see text] disruption, mitochondrial cytochrome [Formula: see text] (cyt [Formula: see text] release, and caspase cascades. Tanshinone IIA treatments effectively decreased H. pylori-induced inflammation and significantly promoted H. pylori-induced intrinsic apoptosis through NF-kB and MAPK (p-38 and JNK) pathways. Tanshinone IIA has great potential as a candidate to protect host cells from H. pylori-induced severe inflammation and gastric cancer.