Cardiovascular diseases (CVDs) are a global health problem. The mortality associated with them is one of the highest. Essentially, CVDs occur when the heart or blood vessels are damaged. Oxidative stress is an imbalance between the production of reactive oxygen species (free radicals) and antioxidant defenses. Increased production of reactive oxygen species can cause cardiac and vascular injuries, leading to CVDs. Antioxidant therapy has been shown to have beneficial effects on CVDs. Plants are a rich source of bioactive antioxidants on our planet. Several classes of these compounds have been identified. Among them, carotenoids and phenolic compounds are the most potent antioxidants. This review summarizes the role of some carotenoids (a/β-carotene, lycopene and lutein), polyphenols such as phenolic acids (caffeic, p-coumaric, ferulic and chlorogenic acids), flavonoids (quercetin, kaempferol and epigallocatechin gallate), and hydroxytyrosol in mitigating CVDs by studying their biological antioxidant mechanisms. Through detailed analysis, we aim to provide a deeper understanding of how these natural compounds can be integrated into cardiovascular health strategies to help reduce the overall burden of CVD.

Breast cancer is a complex disease for which pharmacological treatment does not guarantee success or cure. In addition, current pharmacological therapies induce unwanted side effects due to their lack of specificity or selectivity. Therefore, it is necessary to develop new therapeutic options to improve these aspects. Currently, phytochemicals with antineoplastic properties have been identified from a wide variety of plant sources, and new therapeutic options have been developed based on the conjugation of drugs with polymeric matrices, resulting in nanoparticles or hydrogels with improved properties. Some antineoplastic drugs have been conjugated with antibodies to improve their selectivity and specificity. One of the most important advances in the treatment of breast cancer has been the development of cyclin inhibitors and gene therapy. This review provides an overview of drugs derived from medicinal plants and polymeric matrices with high potential for use in the treatment of breast cancer. We also highlight the clinical evidence for the use of anti-HER2 monoclonal antibodies and cyclin inhibitors in breast cancer, as well as the advantages of using conjugated antibodies. Finally, we mention some considerations that should be taken into account in the search for new therapeutic agents from phytochemicals, polymers, antibodies, cyclin inhibitors, and gene therapy focused on the treatment of breast cancer.

Type 2 diabetes mellitus (T2DM) has been associated with cognitive impairment and an increased risk of dementia in women. This study examined the effects of subchronic metformin treatment on recognition memory and brain pathology in female diabetic mice. T2DM was induced by streptozotocin and nicotinamide injections. Then, the mice received metformin (50, 150, or 250 mg/kg) orally for 28 days. Recognition memory was assessed using the Novel Object Recognition Test (n = 72). Biochemical analyses of whole-brain homogenates evaluated insulin, tau, and insoluble Aβ₄₂ (n = 4). Histological analyses evaluated neuronal damage and amyloid-like deposits in the hippocampal Cornu Ammonis 1 (CA1) region, cerebral cortex, and cerebellum (n = 4). The diabetic mice exhibited hyperglycemia, hyperinsulinemia, dyslipidemia, impaired recognition memory, and neuronal damage. Metformin reduced blood glucose levels and improved recognition memory. Metformin also normalized serum and brain insulin levels and reduced neuronal damage in the CA1 region, cortex, and cerebellum. Metformin reduced cerebellar Congo red-positive amyloid-like deposits and decreased insoluble Aβ₄₂ levels in whole-brain homogenates. However, at 250 mg/kg, metformin increased total and phosphorylated tau levels. These results suggest that metformin mitigates recognition memory deficits, attenuates neuronal damage, and reduces cerebellar amyloid-like deposits in female mice.