Researchers investigate the intricacies of various cellular
processes and pathologies and identify compounds with untapped
therapeutic potential
XI'AN,
China, March 29, 2024 /PRNewswire/ --
Understanding the underlying mechanisms of normal and pathological
cellular processes is essential for developing new drugs.
Fortunately, modern techniques and experimental methods have
greatly accelerated progress. The latest issue of JPA features
three articles in which candidate compounds for treating complex
disorders were successfully identified, alongside their detailed
mechanisms of action.
The first study investigated the use of metformin (Met), a drug
used to manage type II diabetes, for treating benign prostate
hyperplasia (BPH). The article was published in Volume 14, Issue 1
of the journal in January 2024. The
researchers first sought to shed light on how and
which dysregulated sex steroid hormone-related pathways shape
the pathological characteristics of BPH, and whether Met can
restore these pathways.
Through retrospective analysis of data from BPH patients and
clinical assessment of serum and tissue samples, the researchers
identified dihydrotestosterone (DHT) as a major contributor to BPH
among dysregulated sex hormones. DHT promotes prostate cell
proliferation by upregulating androgen receptors and forming
YAP1-TEAD4 heterodimers. In vivo experiments showed that Met
treatment restored sex hormone homeostasis and inhibited
DHT-induced cell proliferation. "Our study provided strong
evidence that Met might be a promising clinical therapeutic
approach for the treatment of BPH," remark corresponding
authors Prof. Qian Lu and Prof.
Xiaoxing Yin.
In the second study, scientists explored the role of epimedin B
(EB), the main flavonoid in the Chinese herb Epimedium
brevicornum Maxim., in melanogenesis. They expanded on previous
findings showing EB's ability to induce melanogenesis and activate
tyrosinase family of proteins (TYRs). Through comprehensive in
vitro and in vivo experiments on human and animal cells,
they uncovered how EB modulated TYRs, increased melanosome numbers,
promoted maturation, and aided depigmentation and repigmentation.
"Our data reveals that EB can stimulate the pigmentation
function of TYRs, which might provide a novel rational strategy for
hypopigmentation treatment in the pharmaceutical and cosmetic
industries," comments corresponding authors Dr. Yiming Li and Prof. Huali Wu.
Finally, in the third study, researchers investigated
ferroptosis, a type of programmed cell death, and its role in nerve
regeneration after peripheral nerve injury (PNI). They found that
oxidative stress at the injury site not only triggered both
apoptosis and ferroptosis in nearby neurons by increasing
intracellular iron via the degradation of ferroportin by UBA52.
Using the Drug Signatures Database, they identified hydralazine
(HYD), a potent arterial vasodilator, as a potential UBA52
disruptor. Early HYD administration after PNI in vivo
expedited axon regeneration and motor function recovery, partly by
suppressing ferroptosis. "The potential clinical implementation
of HYD may lead to a reduction in the prevalence of individuals
with mild symptoms of nerve damage, consequently mitigating the
societal burden," conclude corresponding authors Dr. Bing Xia,
Prof. Zhuojing Luo, and Dr.
Jinghui Huang.
Further studies will hopefully clarify the intricate connections
among cellular processes, diseases, and potential drugs, paving the
way for precise and efficient therapies.
Reference
Titles of original papers
- Metformin: A promising clinSical therapeutical approach
for BPH treatment via inhibiting dysregulated steroid
hormones-induced prostatic epithelial cells proliferation
- Epimedin B exhibits pigmentation by increasing tyrosinase
family proteins expression, activity, and stability
- Hydralazine represses Fpn ubiquitination to rescue injured
neurons via competitive binding to UBA52
Journal: Journal of Pharmaceutical Analysis
DOI
1. https://doi.org/10.1016/j.jpha.2023.08.012
2. https://doi.org/10.1016/j.jpha.2023.09.006
3. https://doi.org/10.1016/j.jpha.2023.08.006
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SOURCE Journal of Pharmaceutical Analysis (JPA)