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| Treatment with Lawsone converts a liver with fibrosis into a healthy liver. Image Credit: Osaka Metropolitan University |
Lawsonia inermis is best known for making henna, a versatile dye that is used to change the color of skin and clothes. Now, researchers from Osaka Metropolitan University have found another use for the pigments extracted from the dye: treating liver disease.
Specifically, they could treat liver fibrosis, a disease that causes excess fibrous scar tissue to build up in the liver as a result of chronic liver injury caused by lifestyle choices such as excessive drinking. Patients with liver fibrosis have increased risks of cirrhosis, liver failure, and cancer. Despite 3–4% of the population having the advanced form of the disease, treatment options remain limited.
One potential treatment for the disease involves hepatic stellate cells (HSCs). Usually, these cells maintain balance in the liver; however, when too many are activated, such as during liver injury, they produce excessive fibrous tissue and collagen, disrupting normal liver function.
A research group led by Associate Professor Tsutomu Matsubara and Dr. Atsuko Daikoku at the Graduate School of Medicine, Osaka Metropolitan University, developed a chemical screening system that identifies substances that directly act on activated HSCs. Using the system, they identified Lawsone, a chemical component from Lawsonia inermis—also known as the henna tree—as a potential inhibitor of HSC activation.
When the researchers administered Lawsone, the mice that received the treatment showed reductions in markers of liver fibrosis, such as YAP, αSMA, and COL1A. They also found upregulated cytoglobin, a marker associated with antioxidant functions in HSCs, suggesting that the HSCs were reverting back toward the non-fibrotic, quiescent type.
The professors believe that by making drugs based on Lawsone, they could create the first treatment that controls and even improves fibrosis. “We are currently developing a drug delivery system capable of transporting drugs to activated HSCs and ultimately hope to make it available for patients with liver fibrosis,” Matsubara said. “By controlling fibroblast activity, including HSCs, we could potentially limit or even reverse the effects of fibrosis.”
Funding: This work was supported by The Osaka City University Glocal hub of wisdom and wellness filled with smiles, The Osaka City University Strategic Research Grant 2017 for young researchers, JSPS KAKENHI Grant Number JP17K18012, JP20K21907, JP21H02626, JP23K21359, JP24K21976, JP15K08314, a Grant for Research Program on Hepatitis from AMED Grant Number JP18fk0210004 and JP19fk0210050.
Published in journal: Biomedicine & Pharmacotherapy
Authors: Atsuko Daikoku, Tsutomu Matsubara, Misako Sato-Matsubara, Miku Ando, Chiho Kadono, Sayuri Takada, Naoshi Odagiri, Hideto Yuasa, Hayato Urushima, Katsutoshi Yoshizato, Norifumi Kawada, and Kazuo Ikeda
Source/Credit: Osaka Metropolitan University
Reference Number: bmed102725_01