Unraveling Tamarindus indica Pulp-Derived Green Magnesium Oxide Nanoparticles for Cardioprotective Potential against Doxorubicin-Induced Cardiomyopathy: A Comprehensive Biochemical and Gene Expression Study.

The present work investigates a sustainable approach to synthesize magnesium oxide nanoparticles (MgO NPs) using an aqueous pulp extract derived from Tamarindus indica. The effective synthesis of MgO NPs was verified by characterizing methods such as UV-vis spectroscopy, X-ray diffraction (XRD), Fourier transform infrared (FT-IR) spectroscopy, and scanning electron microscopy-energy-dispersive X-ray spectroscopy (SEM-EDX). These nanoparticles possess small crystallite sizes, distinctive surface shapes, specific elemental compositions, and stabilizing and encapsulating constituents. Furthermore, total phenolic content (TPC) and total flavonoid content (TFC) tests revealed the existence of phytochemical components in MgO NPs. Significantly, these MgO NPs demonstrated exceptional antioxidant capabilities, as evidenced by their strong performance in antioxidant assays such as 2,2-diphenyl-1-picrylhydrazyl (DPPH), 2,2'-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid) (ABTS), nitric oxide (NO) scavenging, and iron chelation tests. They also exhibited a notable ability to inhibit red blood cell (RBC) hemolysis and lipid peroxidation. In toxicity assessments using Baby Hamster Kidney fibroblasts (BHK-21) and Vero cell lines, the MgO NPs displayed a safe profile. Additionally, in vivo studies on Doxorubicin (DOX)-induced cardiotoxicity revealed the cardioprotective properties of these NPs, accompanied by a detailed understanding of the underlying mechanisms. Pretreatment with MgO NPs effectively countered DOX-induced alterations in cardiac biomarkers, lipid profiles, cardiac enzymes, and lipid peroxidation. Furthermore, they modulated apoptosis-related markers (caspase-3 and p53), upregulated antiapoptotic (Bcl-2), and antioxidant (SOD) markers, suggesting their potential therapeutic value in addressing DOX-induced cardiomyopathy. In conclusion, this study underscores the promising cardioprotective, hypolipidemic, antioxidant, and antiapoptotic qualities of MgO NPs derived from tamarind pulp, offering valuable insights into their therapeutic applications and underlying biological mechanisms.

Biosynthesized magnesium oxide nanoparticles from Tamarindus indica seed attenuate doxorubicin-induced cardiotoxicity by regulating biochemical indexes and linked genes.

The phytochemicals of Tamarindus indica seed hydroalcoholic extract were exploited as a biocatalyst for the sustainable synthesis of magnesium oxide nanoparticles (MgO-NPs). This research investigated the cardioprotective effects of biosynthesized magnesium oxide nanoparticle (MgO-NPs). The biosynthesized seed MgO-NPs were characterized by ultraviolet-visible spectroscopy (UV-Vis), X-ray diffraction (XRD), scanning electron microscopy (SEM) with energy-dispersive X-ray diffraction (EDX), and Fourier-transform infrared spectroscopy (FT-IR). These methodological approaches demonstrated their capacity to synthesize crystalline and aggregated MgO-NPs with a size average of 13.38 ± 0.16 nm. The biogenic MgO-NPs were found to have a significant quantity of total phenolic contents (TPC) and total flavonoid contents (TFC), indicating the existence of phenol and flavonoid-like components. The biogenic MgO-NPs demonstrated a significant free radical scavenging effects compared to different standards as measured by the inhibition of free radicals produced in 2,2-diphenyl-1-picrylhydrazyl (DPPH), 2,2-azinobis-(3-ethylbenzothiazoline-6-sulfonate) (ABTS•+), and Nitric oxide (NO) scavenging methods; they also exhibited higher ferric ion reducing capacity in FRAP assay. Moreover, they were found to be non-toxic in cytotoxic assessment. Pretreatment of Wistar Albino rats with seed MgO-NPs resulted in a significant reduction of cardiac biomarkers, i.e., cardiac Troponin-I (cTnI), creatine kinase (CK-MB), and aspartate aminotransferase (AST). The seed MgO-NPs were more successful in reducing lipid levels. The results of the mRNA expression analysis showed that seed MgO-NPs efficiently reduced the expression of the apoptotic genes p53 and Caspase-3 while restoring the expected levels of SOD gene expression. The histopathological observations were primarily focused on the disruption of cardiac fibers and myofibrillar disintegration, which are consistent with the biochemical findings. Therefore, our research suggests that MgO-NPs derived from the seeds of Tamarindus indica as a powerful antioxidant; the administration may be effective in protecting the heart from DOX-induced cardiotoxicity.

Role of neurotoxicants in the pathogenesis of Alzheimer's disease: a mechanistic insight.

Alzheimer's disease (AD) is the most conspicuous chronic neurodegenerative syndrome, which has become a significant challenge for the global healthcare system. Multiple studies have corroborated a clear association of neurotoxicants with AD pathogenicity, such as Amyloid beta (Aß) proteins and neurofibrillary tangles (NFTs), signalling pathway modifications, cellular stress, cognitive dysfunctions, neuronal apoptosis, neuroinflammation, epigenetic modification, and so on. This review, therefore, aimed to address several essential mechanisms and signalling cascades, including Wnt (wingless and int.) signalling pathway, autophagy, mammalian target of rapamycin (mTOR), protein kinase C (PKC) signalling cascades, cellular redox status, energy metabolism, glutamatergic neurotransmissions, immune cell stimulations (e.g. microglia, astrocytes) as well as an amyloid precursor protein (APP), presenilin-1 (PSEN1), presenilin-2 (PSEN2) and other AD-related gene expressions that have been pretentious and modulated by the various neurotoxicants. This review concluded that neurotoxicants play a momentous role in developing AD through modulating various signalling cascades. Nevertheless, comprehension of this risk agent-induced neurotoxicity is far too little. More in-depth epidemiological and systematic investigations are needed to understand the potential mechanisms better to address these neurotoxicants and improve approaches to their risk exposure that aid in AD pathogenesis.Key messagesInevitable cascade mechanisms of how Alzheimer's Disease-related (AD-related) gene expressions are modulated by neurotoxicants have been discussed.Involvement of the neurotoxicants-induced pathways caused an extended risk of AD is explicited.Integration of cell culture, animals and population-based analysis on the clinical severity of AD is addressed.