Current Pharmaceutical Design - Volume 29, Issue 16, 2023

Hair loss or alopecia is a common dermatological condition affecting up to 2% of the world population. It is often caused by hereditary factors, such as male or female pattern baldness, but it can also result from various environmental factors, an unbalanced diet, or chronic illness. While hair loss is not life-threatening, it can cause significant anxiety, depression, and other psychological problems, ultimately impacting an individual's quality of life. Various treatments for hair loss, including both synthetic drugs, such as minoxidil and finasteride, or medicinal herbs, have been approved by the Food and Drug Administration. Despite synthetic drugs' effectiveness, they may come with potential side effects. Natural remedies have been proposed as a viable option for treating hair loss because many chronic disorders can cause alopecia. As such, this review focuses on identifying alternative, efficient treatment agents with limited side effects. Specifically, it looks into medicinal plants as potential healing agents for treating hair loss. To gather relevant information for the study, multiple databases were searched, including Scopus, PubMed, and Google Scholar. A comprehensive search was conducted using a range of search terms, such as “hair loss”, “alopecia”, “natural remedies for hair loss”, “herbal treatments for hair loss”, and others to extract relevant scientific articles. Many medicinal plants and natural compounds have shown potential in reducing hair loss, thanks to their anti-inflammatory and antioxidant properties and the ability to improve local metabolism when applied externally. According to existing literature, herbal extracts and formulations derived from plants, such as Urtica dioica, Humulus lupulus, Serenoa repens, Vitis vinifera, Pygeum africanum, Cucurbita pepo, etc., as well as certain individual herbal compounds, micronutrients, bee products, and keratin, may be effective in reducing hair loss directly or indirectly. Research suggests that medicinal plants and a variety of natural compounds hold promise in promoting hair growth and preventing alopecia.

Background: Chemotherapy-induced peripheral neuropathy (CIPN) is a painful condition, experienced by patients undergoing chemotherapy with some specific drugs, such as platinum-based agents, taxanes, and vinca alkaloids. Painful CIPN may lead to dose interruptions and discontinuation of chemotherapy and can negatively impact on the quality of life and clinical outcome of these patients. Due to a lack of a practical medical therapy for CIPN, it is necessary to further explore and identify novel therapeutic options. Methods: We have reviewed PubMed and EMBASE libraries to gather data on the mechanism-based pharmacological management of chemotherapy-induced neuropathic pain. Results: This review has focused on the potential mechanisms by which these chemotherapeutic agents may be involved in the development of CIPN, and explains how this may be translated into clinical management. Additionally, we have presented an overview of emerging candidates for the prevention and treatment of CIPN in preclinical and clinical studies. Conclusion: Taken together, due to the debilitating consequences of CIPN for the quality of life and clinical outcome of cancer survivors, future studies should focus on identifying underlying mechanisms contributing to CIPN as well as developing effective pharmacological interventions based on these mechanistic insights.

Background: Neuraminidase is a pathogenic protein of the avian influenza virus. Previous studies have shown that silibinin has the potential to inhibit neuraminidase activity. Objective: This study aims to explore the interaction between silibinin and neuraminidase and the effect of silibinin on the structure and activity of neuraminidase. Methods: In this study, two-dimensional fluorescence spectrum, three-dimensional fluorescence spectrometry, Uv-vis spectroscopy, and circular dichroism analysis were used. Results: Silibinin alters the secondary structure of neuraminidase and inhibits the activity of neuraminidase. Conclusion: Silibinin can interact with neuraminidase and inhibit its activity.

Background: Patients with gastric cancer (GC) are more likely to be infected with 2019 coronavirus disease (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and the prognosis is worse. It is urgent to find effective treatment methods. Objective: This study aimed to explore the potential targets and mechanism of ursolic acid (UA) on GC and COVID-19 by network pharmacology and bioinformatics analysis. Methods: The online public database and weighted co-expression gene network analysis (WGCNA) were used to screen the clinical related targets of GC. COVID-19-related targets were retrieved from online public databases. Then, a clinicopathological analysis was performed on GC and COVID-19 intersection genes. Following that, the related targets of UA and the intersection targets of UA and GC/COVID-19 were screened. Gene Ontology (GO) and Kyoto Encyclopedia of Gene and Genome Analysis (KEGG) pathway enrichment analyses were performed on the intersection targets. Core targets were screened using a constructed protein-protein interaction network. Finally, molecular docking and molecular dynamics simulation (MDS) of UA and core targets were performed to verify the accuracy of the prediction results. Results: A total of 347 GC/COVID-19-related genes were obtained. The clinical features of GC/COVID-19 patients were revealed using clinicopathological analysis. Three potential biomarkers (TRIM25, CD59, MAPK14) associated with the clinical prognosis of GC/COVID-19 were identified. A total of 32 intersection targets of UA and GC/COVID-19 were obtained. The intersection targets were primarily enriched in FoxO, PI3K/Akt, and ErbB signaling pathways. HSP90AA1, CTNNB1, MTOR, SIRT1, MAPK1, MAPK14, PARP1, MAP2K1, HSPA8, EZH2, PTPN11, and CDK2 were identified as core targets. Molecular docking revealed that UA strongly binds to its core targets. The MDS results revealed that UA stabilizes the protein-ligand complexes of PARP1, MAPK14, and ACE2. Conclusion: This study found that in patients with gastric cancer and COVID-19, UA may bind to ACE2, regulate core targets such as PARP1 and MAPK14, and the PI3K/Akt signaling pathway, and participate in antiinflammatory, anti-oxidation, anti-virus, and immune regulation to exert therapeutic effects.

Aim: To investigate the contribution of GAS5 in the pathogenesis of SLE. Background: Systemic Lupus Erythematosus (SLE) is characterized by aberrant activity of the immune system, leading to variable clinical symptoms. The etiology of SLE is multifactor, and growing evidence has shown that long noncoding RNAs (lncRNAs) are related to human SLE. Recently, lncRNA growth arrest-specific transcript 5 (GAS5) has been reported to be associated with SLE. However, the mechanism between GAS5 and SLE is still unknown. Objective: Find the specific mechanism of action of lncRNA GAS5 in SLE. Methods: Collecting samples of the SLE patients, Cell culture and treatment, Plasmid construction, and transfection, Quantitative real-time PCR analysis, Enzyme-linked immunosorbent assay (ELISA), Cell viability analysis, Cell apoptosis analysis, Western blot. Results: In this research, we investigated the contribution of GAS5 in the pathogenesis of SLE. We confirmed that, compared to healthy people, the expression of GAS5 was significantly decreased in peripheral monocytes of SLE patients. Subsequently, we found that GAS5 can inhibit the proliferation and promote the apoptosis of monocytes by over-expressing or knocking down the expression of GAS5. Additionally, the expression of GAS5 was suppressed by LPS. Silencing GAS5 significantly increased the expression of a group of chemokines and cytokines, including IL-1β, IL-6, and THFα, which were induced by LPS. Furthermore, it was identified the involvement of GAS5 in the TLR4-mediated inflammatory process was through affecting the activation of the MAPK signaling pathway. Conclusion: In general, the decreased GAS5 expression may be a potential contributor to the elevated production of a great number of cytokines and chemokines in SLE patients. And our research suggests that GAS5 contributes a regulatory role in the pathogenesis of SLE, and may provide a potential target for therapeutic intervention.

Background: Osteosarcoma is a highly invasive and early metastatic tumor. At present, the toxic and side effects of chemotherapy affect the quality of life of cancer patients to varying degrees. Genipin is an extract of the natural medicine gardenia with various pharmacological activities. Objective: The purpose of this study was to investigate the effect of Genipin on osteosarcoma and its potential mechanism of action. Methods: Crystal violet staining, MTT assay and colony formation assay were used to detect the effect of genipin on the proliferation of osteosarcoma. The effects of vitexin on migration and invasion of osteosarcoma were detected by scratch healing assay and transwell assay. Hoechst staining and flow cytometry were used to detect the effect of genipin on apoptosis of osteosarcoma cells. The expression of related proteins was detected by Western blot. An orthotopic tumorigenic animal model was used to verify the effect of genipin on osteosarcoma in vivo. Results: The results of crystal violet staining, MTT method and colony formation method proved that genipin significantly inhibited the proliferation of osteosarcoma cells. The results of the scratch healing assay and transwell assay showed that gen significantly inhibited the migration and invasion of osteosarcoma cells. The results of Hoechst staining and flow cytometry showed that genipin significantly promoted the apoptosis of osteosarcoma cells. The results of animal experiments show that genipin has the same anti-tumor effect in vivo. Genipin may inhibit the growth of osteosarcoma through PI3K/AKT signaling. Conclusion: Genipin can inhibit the growth of human osteosarcoma cells, and its mechanism may be related to the regulation of PI3K/AKT signaling pathway.