Cosmeceuticals are cosmetic products intended to improve physical appearance, health, beauty and skin ailments. Drugs used to control acne, anti-wrinkle effects, protect from sun burn, improves complexation, delayed effect of ageing and improve skin textures, etc. are comes under category of cosmeceuticals. Cosmeceuticals may be synthetic, natural or hybrid depending upon their compositions. Herbal cosmeceuticals are gaining great attention now a day’s due to their wide range of availability and fewer side effects. There are enormous plants and natural ingredients available commercially as cosmeceuticals. Herbal cosmetics originated naturally from plants, sea, rock salt and soil, etc. Generally herbal cosmetics are free from harmful synthetic chemicals and considered safe to use. Many medicinal plants and herbs offers effect like cosmeceuticals and used extensively for same purpose globally. Natural herbs such as; Neem, Kapoor, Henna, Hirda, Behada, Amalaki, Bringaraj, Rosary Pea and Mandor, etc. are used in cosmetic industry for various purpose. This article presented a descriptive review on Herbal cosmeceuticals.

Mebendazole (MBZ), a benzimidazole anthelmintic and cytoskeleton-disrupting compound, exhibits antitumor properties; however, its action on ovarian cancer (OC) is not clearly understood. This study evaluates the effect of MBZ on OC cell lines OVCAR3 and OAW42, focusing on cell proliferation, migration, invasion, and cancer stemness. The underlying mechanisms, including cytoskeletal disruption, epithelial–mesenchymal transition (EMT), and signaling pathways, were explored. MBZ inhibited OVCAR3 and OAW42 cell proliferation in a dose- and time-dependent manner. Additionally, MBZ significantly impedes migration, spheroid invasion, colony formation, and stemness. In addition, it reduced actin polymerization and down-regulated CSC markers (e.g., CD24, CD44, EpCAM). Moreover, MBZ suppressed MMP-9 activity and inhibited the EMT marker as judged by decreased N-Cadherin and Vimentin and increased E-Cadherin. Furthermore, MBZ induced G2/M cell cycle arrest by modulating Cyclin B1, CDC25C, and WEE1. Also, it triggered apoptosis by disrupting mitochondrial membrane potential. Mechanistic studies revealed a significant downregulation of Girdin, an Akt modulator, along with reduced p-Akt, p-IKKα/β, and p-NF-κB, indicating MBZ’s novel mechanism of action through the Girdin-mediated Akt/IKKα/β/NF-κB signaling axis. Thus, by targeting Girdin, MBZ presents a promising repurposed therapeutic strategy to inhibit cancer cell proliferation and metastasis in ovarian cancer.

Matrix metalloproteinases (MMPs) cleave proteins of extracellular matrix thus facilitating cellular invasion and cancer progression. High MMP-2 activity is frequently reported in several diseases including endometriosis and cancer. Endometriosis, though benign causing pain and infertility, rarely culminate into ovarian cancer. New diagnostic markers are needed for early diagnosis and proper therapeutic avenues since the only diagnostic method is laparoscopy to date. Emerging evidence shows the importance of MMP activity and involvement of noncoding RNA, e.g. miRNA thereon. We investigated the role of miRNA-34a in MMP-2-mediated regulation of invasion and tumorigenesis in endometriosis. Database analysis showed a decreased miRNA-34a in different gynecological malignancies. qRT-PCR with human endometriotic and control tissues revealed a significant elevation in MMP-2 activity with downregulated miR-34a in diseased individuals proving an inverse correlation between miRNA-34a and MMP-2. Luciferase assay in SK-OV-3 cells demonstrated that miRNA-34a-5p directly binds the 3'UTR of the MMP-2 promoter to reduce its transcription followed by suppression of invasion. The zymographic assay also showed a reduced MMP-2 activity upon miR-34a treatment in End1/E6E7 and SK-OV-3 cells. We also found that miRNA-34a-5p inhibits invasion, migration, colony/spheroid formation, and stemness of the cells thereby reducing in vitro tumorigenesis. Subsequently, the immunoblotting results confirmed that MMP-2, and mesenchymal markers like n-cadherin, vimentin, and slug expression were downregulated, whereas the e-cadherin was upregulated in the cells treated with miRNA-34a mimic. Our study demonstrates the direct binding of miR-34a-5p with the MMP-2 gene's 3'UTR and thus repressed its transcription as well as suppressing endometriosis progression.

Background: Ovarian cancer (OC) persists as a major cause of death in gynecological malignancies, primarily due to inherent resistance to chemotherapy and the recurrence of metastatic disease. Aim: This investigation aimed to elucidate a previously uncharacterized mechanism of action for the anthelmintic agent mebendazole (MBZ) in OC cells. Specifically, we aimed to determine if MBZ could simultaneously target mitochondrial function and X-linked inhibitor of apoptosis protein (XIAP), thereby triggering an intrinsic apoptotic pathway. Methods: In vitro studies were conducted using SKOV3 (adenocarcinoma) and PA1 (teratocarcinoma) OC cell lines. Cytotoxicity was assessed via IC ₅₀ determination. Mitochondrial membrane potential (ΔΨm) was evaluated using flow cytometry with rhodamine-123 and confocal microscopy with JC-1 staining. Apoptosis was quantified by annexin V/PI staining. Western blot analysis was used to examine the expression of XIAP, cytochrome c, Bax, and cleaved caspase-3. Molecular docking and density functional theory (DFT) calculations were utilized to investigate MBZ’s interaction with XIAP. Results: MBZ exhibited dose-dependent cytotoxicity in both cell lines (IC ₅₀ : 1.25 µM in SKOV3, 0.312 µM in PA1), with PA1 showing greater sensitivity. Significant ΔΨm depolarization was observed (40% in SKOV3, 33% in PA1), accompanied by increased JC-1 monomer/aggregate ratios (5.7-9.9-fold). MBZ induced apoptosis without significant necrosis (3.2-4.5-fold increase in Annexin V ⁺ cells). Mechanistically, MBZ reduced XIAP expression (2.5-fold) and upregulated cytochrome c, Bax, and cleaved caspase-3. Molecular docking revealed high-affinity binding of MBZ to the XIAP BIR3 domain, comparable with A4E (ASTX660), with unique interactions at LYS299. DFT calculations confirmed MBZ’s comparable electronic properties, including a lower Highest Occupied Molecular Orbital-Lowest Unoccupied Molecular Orbital energy gap relative to A4E. Conclusion: This study identifies a novel dual mode of action for MBZ in OC cells, concurrently disrupting mitochondrial function and directly inhibiting XIAP, leading to caspase-dependent apoptosis. This unique mechanism of action suggests MBZ as a promising repurposed therapeutic strategy to potentially overcome chemoresistance in OC.

The pharmaceutical industry has increasingly turned to natural product-based drug development as synthetic drug discovery declines. Marine ecosystems have become a key source of novel therapeutic agents, known as marine natural products (NPs), celebrated for their unique chemical structures and diverse biological activities. This chapter comprehensively explores marine NPs as a rich source of pharmacologically active compounds. We discuss the shift towards natural product-based drugs, the growing focus on marine ecosystems, and the diverse pharmacological actions of marine NPs. We also classify these natural products based on their sources. Furthermore, the chapter highlights marine NPs that are in various phases of clinical trials, those approved, and those already marketed as drugs. We emphasize the translational potential of marine NPs, showcasing their journey from promising leads to clinically relevant drugs, underscoring their importance as a reservoir of bioactive compounds.