Unveiling the versatility of gelatin methacryloyl hydrogels: a comprehensive journey into biomedical applications.

Gelatin methacryloyl (GelMA) hydrogels have gained significant recognition as versatile biomaterials in the biomedical domain. GelMA hydrogels emulate vital characteristics of the innate extracellular matrix by integrating cell-adhering and matrix metalloproteinase-responsive peptide motifs. These features enable cellular proliferation and spreading within GelMA-based hydrogel scaffolds. Moreover, GelMA displays flexibility in processing, as it experiences crosslinking when exposed to light irradiation, supporting the development of hydrogels with adjustable mechanical characteristics. The drug delivery landscape has been reshaped by GelMA hydrogels, offering a favorable platform for the controlled and sustained release of therapeutic actives. The tunable physicochemical characteristics of GelMA enable precise modulation of the kinetics of drug release, ensuring optimal therapeutic effectiveness. In tissue engineering, GelMA hydrogels perform an essential role in the design of the scaffold, providing a biomimetic environment conducive to cell adhesion, proliferation, and differentiation. Incorporating GelMA in three-dimensional printing further improves its applicability in drug delivery and developing complicated tissue constructs with spatial precision. Wound healing applications showcase GelMA hydrogels as bioactive dressings, fostering a conducive microenvironment for tissue regeneration. The inherent biocompatibility and tunable mechanical characteristics of GelMA provide its efficiency in the closure of wounds and tissue repair. GelMA hydrogels stand at the forefront of biomedical innovation, offering a versatile platform for addressing diverse challenges in drug delivery, tissue engineering, and wound healing. This review provides a comprehensive overview, fostering an in-depth understanding of GelMA hydrogel's potential impact on progressing biomedical sciences.

Research on Alzheimer's Disease (AD) Involving the Use of In vivo and In vitro Models and Mechanisms.

BACKGROUND: Alzheimer's Disease (AD) is a neurodegenerative disorder characterized by the progressive formation of extracellular amyloid plaques, intracellular neurofibrillary tangles, inflammation, and impaired antioxidant systems. Early detection and intervention are vital for managing AD effectively. OBJECTIVE: This review scrutinizes both in-vivo and in-vitro screening models employed in Alzheimer's disease research. In-vivo models, including transgenic mice expressing AD-related mutations, offer profound insights into disease progression and potential therapeutic targets. A thorough understanding of these models and mechanisms will facilitate the development of novel therapies and interventions for Alzheimer's disease. This review aims to provide an overview of the current experimental models in AD research, assess their strengths and weaknesses as model systems, and underscore the future prospects of experimental AD modeling. METHODS: We conducted a systematic literature search across multiple databases, such as Pub- Med, Bentham Science, Elsevier, Springer Nature, Wiley, and Research Gate. The search strategy incorporated pertinent keywords related to Alzheimer's disease, in-vivo models, in-vitro models, and screening mechanisms. Inclusion criteria were established to identify studies focused on in-vivo and in-vitro screening models and their mechanisms in Alzheimer's disease research. Studies not meeting the predefined criteria were excluded from the review. RESULTS: A well-structured experimental animal model can yield significant insights into the neurobiology of AD, enhancing our comprehension of its pathogenesis and the potential for cutting-edge therapeutic strategies. Given the limited efficacy of current AD medications, there is a pressing need for the development of experimental models that can mimic the disease, particularly in pre-symptomatic stages, to investigate prevention and treatment approaches. To address this requirement, numerous experimental models replicating human AD pathology have been established, serving as invaluable tools for assessing potential treatments. CONCLUSION: In summary, this comprehensive review underscores the pivotal role of in-vivo and in-vitro screening models in advancing our understanding of Alzheimer's disease. These models offer invaluable insights into disease progression, pathological mechanisms, and potential therapeutic targets. By conducting a rigorous investigation and evaluation of these models and mechanisms, effective screening and treatment methods for Alzheimer's disease can be devised. The review also outlines future research directions and areas for enhancing AD screening models.

Preventive effect of Metformin against N-nitrosodiethylamine-initiated hepatocellular carcinoma in rats.

Effect of Metformin in chemically induced hepatocarcinogenesis was assessed in Wistar rats. Intraperitoneal administration of chemical carcinogen diethyl nitrosamine (DENA) (200 mg/kg) in single dose elevated the levels of serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), alkaline phosphatase (ALP), total cholesterol (TC), triglycerides (TG) and reduced high density lipoproteins (HDL), total proteins (TPR) and blood glucose level in tested animals. Histopathological examinations of the liver tissue showed marked carcinogenicity of the chemical carcinogen. Food and water intake, animal weights and serum albumin (ALB) were also assessed. The animals exposed to DENA showed a significant decrease in the body weights and, there were no significant alterations found in the total bilirubin (TBR) levels and gamma-glutamyltranspeptidase (GGTP), whereas the decreased levels of serum ALB were maintained by Metformin treatment. The elevated levels of serum SGOT, SGPT, ALP, AFP, TC and TG were restored by administration of Metformin in reduced dose (125 mg/kg) daily for 16 weeks p.o. Physiological and biochemical analysis showed the beneficial effects of Metformin in the animals exposed to DENA.