The simplification of current hepatitis C diagnostic algorithms and the emergence of digital diagnostic devices will be very crucial to achieving the WHO’s set goals of hepatitis C diagnosis (i.e., 90%) by 2030. From the last decade, hepatitis C diagnosis has been revolutionized by the advent and approval of state-of-the-art HCV diagnostic platforms which have been efficiently implemented in high-risk HCV populations in developed nations as well as in some low-to-middle income countries (LMICs) to identify millions of undiagnosed hepatitis C-infected individuals. Point-of-care (POC) rapid diagnostic tests (RDTs; POC-RDTs), RNA reflex testing, hepatitis C self-test assays, and dried blood spot (DBS) sample analysis have been proven their diagnostic worth in real-world clinical experiences both at centralized and decentralized diagnostic settings, in mass hepatitis C screening campaigns, and hard-to-reach aboriginal hepatitis C populations in remote areas. The present review article overviews the significance of current and emerging hepatitis C diagnostic packages to subvert the public health care burden of this ‘silent epidemic’ worldwide. We also highlight the challenges that remain to be met about the affordability, accessibility, and health system-related barriers to overcome while modulating the hepatitis C care cascade to adopt a ‘test and treat’ strategy for every hepatitis C-affected individual. We also elaborate some key measures and strategies in terms of policy and progress to be part of hepatitis C care plans to effectively link diagnosis to care cascade for rapid treatment uptake and, consequently, hepatitis C cure.

Background: Liver cancer is the sixth most prevalent form of cancer and the second major cause of cancer-associated mortalities worldwide. Cancer nanotechnology has the ability to fundamentally alter cancer treatment, diagnosis, and detection. Objective: In this study, we explained the development of graphene oxide/polyethylene glycol/folic acid/brucine nanocomposites (GO/PEG/Bru-FA NCs) and evaluated their antimicrobial and anticancer effect on the liver cancer HepG2 cells. Methodology: The GO/PEG/Bru-FA NCs were prepared using the co-precipitation technique and characterized using various techniques. The cytotoxicity of the GO/PEG/Bru-FA NCs was tested against both liver cancer HepG2 and non-malignant Vero cells using an MTT assay. The antimicrobial activity of the GO/PEG/Bru-FA NCs was tested against several pathogens using the well diffusion technique. The effects of GO/PEG/Bru-FA NCs on endogenous ROS accumulation, apoptosis, and MMP levels were examined using corresponding fluorescent staining assays, respectively. The apoptotic protein expressions, such as Bax, Bcl-2, and caspases, were studied using the corresponding kits. Results: The findings of various characterization assays revealed the development of GO/PEG/Bru-FA NCs with face-centered spherical morphology and an agglomerated appearance with an average size of 197.40 nm. The GO/PEG/Bru-FA NCs treatment remarkably inhibited the growth of the tested pathogens. The findings of the MTT assay evidenced that the GO/PEG/Bru-FA NCs effectively reduced the HepG2 cell growth while not showing toxicity to the Vero cells. The findings of the fluorescent assay proved that the GO/PEG/Bru-FA NCs increased ROS generation, reduced MMP levels, and promoted apoptosis in the HepG2 cells. The levels of Bax, caspase-9, and − 3 were increased, and Bcl-2 was reduced in the GO/PEG/Bru-FA NCs-treated HepG2 cells. Conclusion: The results of this work demonstrate that GO/PEG/Bru-FA NCs suppress viability and induce apoptosis in HepG2 cells, indicating their potential as an anticancer candidate.

Background/Objectives: Pulmonary fibrosis (PF) is a progressive interstitial lung disease with limited therapeutic options. Lepidium sativum (cress seeds) possess recognized antioxidant and anti-inflammatory properties, yet its potential antifibrotic activity has not been investigated. This study evaluated the phytochemical composition and antifibrotic efficacy of cress seed extract (CSE) and examined whether its effects are associated with modulation of the ncNRFR/let-7d pathway in methotrexate (Mtx)-induced PF. Methods: Comprehensive metabolite profiling was performed using GC–MS, HPLC, and UPLC–T-TOF–MS/MS. Antioxidant capacity and antiproliferative effects were assessed in vitro. Network pharmacology was used to identify CSE-related PF targets and regulatory pathways. In vivo, PF was induced in adult male Wistar rats by Mtx, followed by oral CSE administration (50–150 mg/kg). Biochemical markers of inflammation, oxidative stress, extracellular matrix deposition, EMT, and ncRNA expression (ncNRFR and let-7d) were quantified alongside histopathology and immunohistochemistry. Results: CSE contained diverse terpenes, phenolics, flavonoids, glucosinolates, and amino acid derivatives. It exhibited potent antioxidant activity and antiproliferative effects against A549 and Hep2 lung cancer cells. Network analysis identified 997 overlapping CSE–PF targets and highlighted IL6 and MMP1 as relevant miR-let-7d–associated nodes. In vivo, Mtx-induced marked fibrosis characterized by increased ncNRFR, reduced let-7d, elevated IL6, HMGB1, TGF-β, MMP1, collagen, and hydroxyproline, and reduced antioxidant enzyme activity. CSE treatment dose-dependently mitigated these alterations, improved histoarchitecture, and reduced collagen deposition. Conclusions: CSE showed antifibrotic, antioxidant, and anti-inflammatory activity in MTX-induced PF in rats and modulated the reciprocal expression patterns of ncNRFR and let-7d. These findings support CSE as a potential source of bioactive constituents for PF management and identify the putative ncNRFR–let-7d regulatory relationship as a novel pathway in fibrotic lung disease, warranting further mechanistic investigation.