Emodin, a plant compound used in traditional Chinese medicine, has potent anti-inflammatory and anti-rheumatic properties that, when combined with autophagy inhibitors, may be a promising therapeutic strategy to alleviate symptoms of ankylosing spondylitis, a study reports.

The study, “ Emodin induces apoptosis and autophagy of fibroblasts obtained from patient with ankylosing spondylitis ,” was published in Drug, Design, Development and Therapy.

Ankylosing spondylitis (AS) is a debilitating type of arthritis that mainly affects the joints of the spine, causing chronic pain and lifelong physical disability.

Recent studies have shown the excessive growth of fibroblasts — connective tissue cells that produce a protein called collagen, a compound present in the network that surrounds and supports cells as they grow — might be involved in AS development.

Emodin, a chemical compound extracted from the roots of a plant commonly known as Chinese rhubarb (Rheum palmatum), has been shown to possess strong anti-inflammatory, anti-rheumatic, anti-cancer and anti-viral properties. Because of these properties, emodin could be an interesting therapeutic candidate for AS and other types of rheumatic disorders.

In this study, a team of Chinese researchers tested the therapeutic potential of emodin in lab-cultured fibroblasts from AS patients.

The study enrolled a total of 40 AS patients — 25 men and 15 women — between April 2017 and May 2018. Fibroblasts were isolated from patients during surgery and then placed in a lab dish to test the effects of emodin treatment.

Results showed that emodin prevented fibroblasts’ excessive growth and induced apoptosis (controlled cell death) by increasing the activity and levels of pro-apoptotic proteins (caspase-9, caspase-3, and Bax) and decreasing levels of anti-apoptotic proteins (Bcl-2).

In addition, emodin treatment also boosted fibroblasts’ autophagy — a process where cells degrade or recycle components that are damaged or no longer needed — by increasing the levels of autophagy proteins (Atg12, Atg5, and Beclin 1).

As expected, combined treatment with the autophagy inhibitor 3-methyladenine (3MA) fully blocked the autophagy boost effect triggered by emodin. Conversely, 3MA treatment enhanced fibroblasts’ controlled cell death brought about by emodin.

“These results indicated that inhibition of autophagy possibly aggravated DNA damage in fibroblasts obtained from patients with AS, sequentially leading to fibroblast cell death,” in other words, by preventing fibroblasts from repairing internal components through autophagy, researchers managed to boost fibroblasts’ apoptosis triggered by emodin treatment.

“In conclusion, we suggest that a combination of emodin and autophagy inhibitors could be a potent method for improving the symptoms of AS in the future,” researchers said.