Home | About PM | Editorial board | Search | Ahead of print | Current Issue | Archives | Instructions | Subscribe | Advertise | Contact us |  Login 
Pharmacognosy Magazine
Search Article 
  
Advanced search 
 
ORIGINAL ARTICLE
Year : 2021  |  Volume : 17  |  Issue : 74  |  Page : 334-341

Lappaconitine hydrochloride induces apoptosis and S phase cell cycle arrest through MAPK signaling pathway in human liver cancer HepG2 cells


1 College of Life Science, Northwest Normal University, Lanzhou, China
2 Key Laboratory of Stem Cells and Gene Drug of Gansu Provincial, The 940th Hospital of Joint Logistics Support Force of Chinese People's Liberation Army, Lanzhou, China
3 School of Pharmacy, Lanzhou University, Lanzhou, China
4 Gansu Provincial Academy of Medical Sciences, Gansu Provincial Cancer Hospital, Lanzhou, China

Correspondence Address:
Junyi Ma
College of Life Science, Northwest Normal University, Lanzhou 730070
China
Ling Hui
Key Laboratory of Stem Cells and Gene Drug of Gansu Provincial, The 940th Hospital of Joint Logistics Support Force of Chinese People's Liberation Army, Lanzhou 730050
China
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/pm.pm_251_20

Rights and Permissions

Background: Lappaconitine (LA), isolated from the root of Aconitum sinomontanum Nakai, had definite pharmacological effects, such as anticancer, analgesia, and anti-inflammation. LA and its derivatives had garnered prevalent consideration due to its analgesic and antitumor effects, but its clinical application was constrained by poor solubility. In this study, a novel LA hydrochloride (LH) was synthesized to upsurge the solubility and improve the efficacy. Objectives: The objective of this study was to examine the antitumor effect and primary mechanisms of LH on cell proliferation, cell cycle, and apoptosis in HepG2 cells. Materials and Methods: The cell viability and proliferation were assessed using Cell Counting Kit-8 and 5'-ethynyl-2'-deoxyuridine assay. The apoptosis morphological feature of cell was detected with the 4',6-diamidino-2-phenylindole (DAPI) staining method. The effect of protein expression levels was recognized by Western blot assay. Cell cycle and apoptosis were estimated using flow cytometer. Results: LH repressed cell viability and proliferation of HepG2 cells and persuaded apoptosis in a dose-dependent way. Flow cytometry analysis results display that LH could arrest cell cycle of HepG2 cells in S phase, thereby preventing cells entering G2/M phase. LH upregulated the expression of cytochrome C, Bax, P53, cleaved caspase-3, cleaved caspase-9, and cleaved poly ADP-ribose polymerase (PARP) and suppressed the expression of Bcl-2. Furthermore, caspase inhibitor z-VAD-fmk inhibited the activation of cleaved caspase-3 and cleaved caspase-9. Moreover, LH abridged the phosphorylation levels of extracellular signal-regulated kinase and augmented the phosphorylation levels of c-Jun N-terminal kinase and P38. Conclusion: LH designated antitumor effect against HepG2 cells through suppressing cell proliferation, inducing apoptosis and cell cycle arrest by aiming mitogen-activated protein kinase signaling pathway.


[FULL TEXT] [PDF]*
Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed140    
    Printed0    
    Emailed0    
    PDF Downloaded24    
    Comments [Add]    

Recommend this journal