NDLI: Ninjinyoeito ameliorated cigarette smoke extract-induced apoptosis and inflammation through JNK signaling inhibition in human lung fibroblasts

Content Provider	Springer Nature : BioMed Central
Author	Murata, Kenta Fujita, Nina Takahashi, Ryuji
Abstract	Background Cigarette smoke is a major risk factor for various lung diseases, such as chronic obstructive pulmonary disease (COPD). Ninjinyoeito (NYT), a traditional Chinese medicine, has been prescribed for patients with post-illness or post-operative weakness, fatigue, loss of appetite, rash, cold limbs, and anemia. In addition to its traditional use, NYT has been prescribed for treating frailty in gastrointestinal, respiratory, and urinary functions. Further, NYT treatment can ameliorate cigarette smoke-induced lung injury, which is a destructive index in mice; however, the detailed underlying mechanism remains unknown. The purpose of this study was to investigate whether NYT ameliorates cigarette smoke-induced cell injury and inflammation in human lung fibroblasts and determine its mechanism of action. Methods We prepared a cigarette smoke extract (CSE) from commercially available cigarettes to induce cell injury and inflammation in the human lung fibroblast cell line HFL1. The cells were pretreated with NYT for 24 h prior to CSE exposure. Cytotoxicity and cell viability were measured by lactate dehydrogenase (LDH) cytotoxicity assay and cell counting kit (CCK)-8. IL-8 level in the cell culture medium was measured by performing Enzyme-Linked Immuno Sorbent Assay (ELISA). To clarify the mechanisms of NYT, we used CellROX Green Reagent for reactive oxygen species (ROS) production and western blotting analysis for cell signaling. Results Exposure of HFL1 cells to CSE for 24 h induced apoptosis and interleukin (IL)-8 release. Pretreatment with NYT inhibited apoptosis and IL-8 release. Furthermore, CSE exposure for 24 h increased the production of ROS and phosphorylation levels of p38 and JNK. Pretreatment with NYT only inhibited CSE-induced JNK phosphorylation, and not ROS production and p38 phosphorylation. These results suggest that NYT acts as a JNK-specific inhibitor. Conclusion NYT treatment ameliorated CSE-induced apoptosis and inflammation by inhibiting the JNK signaling pathway. Finally, these results suggest that NYT may be a promising therapeutic agent for patients with COPD.
Related Links	https://bmccomplementmedtherapies.biomedcentral.com/counter/pdf/10.1186/s12906-022-03574-5.pdf
Ending Page	10
Page Count	10
Starting Page	1
File Format	HTM / HTML
ISSN	26627671
DOI	10.1186/s12906-022-03574-5
Journal	BMC Complementary Medicine and Therapies
Issue Number	1
Volume Number	22
Language	English
Publisher	BioMed Central
Publisher Date	2022-03-31
Access Restriction	Open
Subject Keyword	Complementary & Alternative Medicine Internal Medicine Chiropractic Medicine Ninjinyoeito JNK Apoptosis Cigarette smoke
Content Type	Text
Resource Type	Article
Subject	Complementary and Alternative Medicine
Journal Impact Factor	3.3/2023
5-Year Journal Impact Factor	3.6/2023

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