Glycerol extract of Water hyacinth (Eichhornia crassipes (Mart.) Solms) attenuates hydrogen peroxide (H2O2)-induced cell death in HT22 hippocampal neurons

Abstract

Neurological disorders continue to represent a significant global health burden, ranking among the leading causes of mortality and long-term disability. The persistent lack of effective therapeutic interventions reflects an incomplete understanding of the complex molecular mechanisms underlying neuronal cell death in the diseased brain. Among these, oxidative stress has been identified as a critical secondary injury mechanism that exacerbates neuronal damage. Recently, Eichhornia crassipes (Mart.), commonly known as water hyacinth, has emerged as a promising source of bioactive compounds with notable anti-inflammatory and antioxidant properties, making it a potential candidate for the development of neuroprotective therapies. This study aimed to assess the neuroprotective potential of E. crassipes extracts (ultrasound-assisted maceration), with glycerol extract (GE) emerging as the most effective extract, using a cell-based model of oxidative stress-induced by hydrogen peroxide (H₂O₂) in hippocampal HT22 cells. Cell viability of HT22 cells were measured through MTT assay, in order to determine cytotoxicity of extracts (0.5 mg/ml – 5 mg/ml) and protective effects of the extracts against H₂O₂ (via co-treatment assay). Our study revealed that H₂O₂ was able to induce cell viability loss in HT22 cells in a dose-dependent manner, and the IC₅₀ value of H₂O₂ was determined as approximately 655.3 µM. Following the co-treatment assay, GE at 0.8 mg/ml displayed a significant protective effect by alleviating H₂O₂ (700 µM)-induced cell death as compared to the H₂O₂ alone group (67.4 ± 4.4% viability vs. 52.4 ± 1.4%, p < 0.05), while aqueous and mixed extracts did not display significant protective trend. These preliminary findings suggest that glycerol-based E. crassipes extract possesses underexplored neuroprotective potential against H₂O₂-induced oxidative stress in neuronal cells, though further mechanistic and in vivo investigation are required to validate these effects and establish translation relevance.