The development of therapies followed a generalized approach for a long time, assuming that a single treatment could effectively address various patient populations. However, recent breakthroughs have revealed the limitations of this one-size-fits-all paradigm. More recently, the field of therapeutics has witnessed a shift towards other modules, including cell therapies, high molecular weight remedies, personalized medicines, and gene therapies. Such advancements in therapeutic modules have the potential to revolutionize healthcare and pave the way for medicines that are more efficient and with minimal side effects. Cell therapies have gained considerable attention in regenerative medicine. Stem cell-based therapies, for instance, hold promise for tissue repair and regeneration, with ongoing research focusing on enhancing their efficacy and safety. High molecular weight drugs like peptides and proteins emerged as promising therapeutics because of their high specificity and diverse biological functions. Engineered peptides and proteins are developed for targeted drug delivery, immunotherapy, and disease-modulation. In personalized-medicine, tailored treatments to individuals based on specific genetic profiling, lifestyle, biomarkers, and disease characteristics are all implemented. Clinicians have tailored treatments to optimize outcomes and minimize adverse effects, using targeted therapies based on specific mutations, yielding remarkable results. Gene therapies have revolutionized the treatment of genetic disorders by directly targeting the underlying genetic abnormalities. Innovative techniques such as CRISPR-Cas9 have allowed precise gene editing, opening up possibilities for curing previously incurable conditions. In conclusion, advancements in therapeutic modules have the potential to revolutionize healthcare and pave the way for medicines that are more efficient and with minimal side effects.

We examined whether Nigella sativa (NS) oil and its active constituent thymoquinone (TQ) attenuate oxidative stress in the heart and brain in an experimental model of diabetes mellitus using streptozotocin (STZ). Oxidative stress was assessed by measuring cardiac and brain nitric oxide (NO), lipid peroxide levels, glutathione (GSH) and antioxidant enzyme activities, i.e. glutathione-S-transferase (GST) and catalase. Cardiac metabolic damage was estimated by measuring cardiac creatine kinase muscle and brain types (CK-MB). Brain monoamine levels were also evaluated. STZ diabetes induced a significant increase in heart and brain NO and malondialdehyde concentrations compared with the control group. These changes were attenuated by posttreatment of rats with NS oil and TQ. STZ diabetes induced oxidative stress via a significant decrease in GST, GSH and catalase. These lowered levels were improved by either NS oil or TQ administration. Serum CK-MB was decreased in the diabetic rats, which recovered with NS oil and TQ administration. During the course of diabetes, there was a marked increase in norepinephrine and dopamine concentrations and a marked decrease in serotonin concentration compared to the control group. These findings were partly reversed by oral administration of either NS oil or TQ. It is concluded that NS and TQ correct STZ-diabetes-induced alterations in CK-MB and brain monoamines due to their antioxidant properties.

Breast cancer (BC) represents one of the most prevalent malignant threats to women globally. Tumor relapse or metastasis is facilitated by BC stemness progression, contributing to tumorigenicity. Therefore, comprehending the characteristics of stemness progression and the underlying molecular mechanisms is pivotal for BC advancement. Hinokitiol (β-thujaplicin), a tropolone-related compound abundant in the heartwood of cupressaceous plants, exhibits antimicrobial activity. In our study, we employed three BC cell lines (MDA-MB-231, MCF-7, and T47D) to assess the expression of stemness-, apoptosis-, and autophagy-related proteins. Hinokitiol significantly reduced the viability of cancer cells in a dose-dependent manner. Furthermore, we observed that hinokitiol enhances apoptosis by increasing the levels of cleaved poly-ADP-ribose polymerase (PARP) and phospho-p53. It also induces dysfunction in autophagy through the upregulation of LC3B and p62 protein expression. Additionally, hinokitiol significantly suppressed the number and diameter of cancer cell line spheres by reducing the expression of cluster of differentiation44 (CD44) and key transcription factors. These findings underscore hinokitiol’s potential as a therapeutic agent for breast cancer, particularly as a stemness-progression inhibitor. Further research and clinical studies are warranted to explore the full therapeutic potential of hinokitiol in the treatment of breast cancer.