ABSTRACT
Background: Rheumatoid arthritis fibroblast-like synovial cells (RA-FLS) have become the core effector cells for the progression of rheumatoid arthritis due to their "tumor-like cell" characteristics, such as being able to break free from growth restrictions caused by contact inhibition, promoting angiogenesis, invading surrounding tissues, and leading to uncontrolled synovial growth. In recent years, cold air plasma (CAP) has been widely recognized for its clear anticancer effect. Inspired by this, this study investigated the inhibitory effect of CAP on the tumor-like biological behavior of RA-FLS through in vitro experiments. Methods: Treatment of RA-FLS with CAP at different time doses (0s, 30s, 60s, 120s). 5-ethynyl-2'-deoxyuridine (EdU) proliferation assay was used to determine the cell viability. Analysis of cell migration and invasion was performed by wound-healing assay, transwell assay and immunofluorescent staining for f-actin, respectively. Flow cytometry technique was used for analysis of cell cycle and determination of reactive oxygen species (ROS). Hoechst staining was used for analysis of cell apoptosis. Protein expression was analyzed by Western blot analysis. Results: Molecular and cellular level mechanisms have revealed that CAP blocks RA-FLS in the G2/M phase by increasing intracellular reactive oxygen species (ROS), leading to increased apoptosis and significantly reduced migration and invasion ability of RA-FLS. Conclusion: Overall, CAP has significant anti proliferative, migratory, and invasive effects on RA-FLS. This study reveals a new targeted treatment strategy for RA.
ABSTRACT
Rheumatoid arthritis (RA) has plagued physicians and patients for years due to the lack of targeted treatment. In this study, inspired by the commonality between rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS) and cancer cells, the therapeutic effects of cold air plasma (CAP) on RA are studied systematically and thoroughly. In/ex vivo results show that CAP with the proper dosage significantly relieves symptoms including synovial hyperplasia, inflammatory infiltration, and angiogenesis and eliminates the root cause by triggering the self-antioxidant capability of the surrounding tissue. The mechanism on the molecular and cellular level is also revealed that the spontaneous reactive oxygen species (ROS) cascade induces the mitochondrial apoptosis pathway on RA-FLS. This study reveals a new strategy for targeted treatment of RA and the mechanistic study provides the theoretical foundation for future development of plasma medicine.
ABSTRACT
Introduction: Transvenous embolization (TVE) has been proven to be safe and feasible as an alternative management of brain arteriovenous malformations (AVMs). We presented four patients with a hemorrhagic brain AVM who underwent TVE and reviewed the relevant literature. Methods: Four patients underwent TVE of a hemorrhagic brain AVM in our center between July 2019 and July 2020. We retrospectively collected and analyzed the clinical and imaging data of these patients and those reported in previously published studies. Results: Four patients with a hemorrhagic brain AVM were included. Nidus sizes ranged from 0.79 to 2.56 cm. Spetzler-Martin grade ranged from grade II to grade III. The AVM nidus was located in a deep brain region in three patients. One patient underwent TVE alone and three underwent combined transarterial and transvenous approaches. Digital subtraction angiography (DSA) demonstrated complete obliteration of the vascular malformation after embolization in all four patients. Three patients were independent [modified Rankin Scale (mRS) score ≤ 2] at discharge. All four patients were independent at the last follow-up. AVM obliteration was confirmed in all four patients at the last angiographic follow-up. Conclusion: Transvenous embolization can be used as an alternative treatment for contemporary management of brain AVMs, appropriate patient selection is essential to achieve a good clinical outcome.
