Hypericin-photodynamic therapy inhibits proliferation and induces apoptosis in human rheumatoid arthritis fibroblast-like synoviocytes cell line MH7A

نویسندگان

1 Faculty of Graduate Studies, Hunan University of Chinese Medicine, Changsha 410208, Hunan Province, China

2 Department of Orthopedics, No. 91 Central hospital of Liberation Army, Jiaozuo 454150, Henan province, China

3 Department of Orthopedics, Luoyang Orthopedic Hospital of Henan Province, Luoyang 471000, Henan Province, China

4 Department of Orthopedics, Luoyang Orthopedic Hospital of Henan Province, Luoyang 471000, Henan Province, China

5 Department of Orthopedics, No. 91 Central hospital of Liberation Army, Jiaozuo 454150, Henan province, China

6 Department of Orthopedics, Luoyang Orthopedic Hospital of Henan Province, Luoyang 471000, Henan Province, China

7 Department of Orthopedics, Luoyang Orthopedic Hospital of Henan Province, Luoyang 471000, Henan Province, China

8 Department of Orthopedics, Luoyang Orthopedic Hospital of Henan Province, Luoyang 471000, Henan Province, China

9 Department of Orthopedics, Luoyang Orthopedic Hospital of Henan Province, Luoyang 471000, Henan Province, China

doi
10.22038/ijbms.2018.23871.5991
چکیده

Objective(s): To elucidate the effects and potential mechanisms of hypericin-photodynamic therapy (HYP-PDT) for treating the human rheumatoid arthritis (RA) fibroblast-like synoviocyte (FLS) MH7A cell-line. Materials and Methods: MH7A cells were subjected to HYP-PDT intervention and apoptosis was evaluated via MTT, nuclear staining, and flowcytometry analyses. Intracellular reactive oxygen species (ROS) were measured with the fluorescent probe 2’7’-dichlorofluorescein diacetate (DCFH-DA). To verify the effects of HYP on apoptotic and nuclear factor kappa-B (NF-κB) pathways, caspase-8, 9, poly-ADP-ribose polymerase (PARP), phosphorylated (p)-NF-κB p65, NF-κB p65 and p-IκBα protein expressions were quantified with western blot. Quantitative real-time PCR was used to assay NF-κB p65 mRNA. Results: HYP-PDT inhibited MH7A cell viability and induced apoptosis in a dose-dependent manner. Meanwhile, intracellular ROS levels increased significantly after HYP-PDT treatment. Furthermore, the expression of cleaved caspase-9 and PARP was increased by HYP-PDT treatment, with a concurrent decline in NF-κB. Conclusion: HYP-PDT induces apoptosis in MH7A cells, at least partially, via generation of ROS, regulation of the apoptotic pathway and suppression of the NF-κB pathway. These findings suggest that HYP-PDT may be a potential treatment for RA.