Table 2.
Effects of HT and derivatives in in vitro neurodegenerative and Parkinson’s disease models.
| Study | In Vitro Model | Compounds Tested | Concentrations | Significant Outcomes | Ref. |
|---|---|---|---|---|---|
| Yu et al., 2016 | SH-SY5Y cells treated with 6-OHDA | HT | 20–90 µM | Induction of the expression of phase II detoxifying enzymes NQO1, GST, GCL, and HO-1. | [30] |
| Crespo et al., 2017 | Astrocytic cell line C6 exposed to Aβ (25–35) | HT | 5 µM | Prevention of viability decrease through increased Akt activation. | [31] |
| Omar et al., 2017 | SH-SY5Y cells treated with copper and H2O2 | HT | 10–50 μM | Antiradical and protective activity against peroxidation. | [29] |
| Funakohi-Tago et al., 2018 | SH-SY5Y cells treated with 6-OHDA | HT, HT acetate and HT butyrate | 5–10 µM | Reduction in the 6-OHDA-induced generation of ROS, activation of caspase-3, and subsequent cell death by HT butyrate, but not HT or HT acetate. HT butyrate induced Nrf2 and HO-1 expression | [32] |
| Hornedo-Ortega et al., 2018 | Rat pheochromocytoma PC12 cells | HT | 25–200 µM | Inhibition of α-synuclein fibrils formation and of their pro-inflammatory activity. | [33] |
| Lopez de Las Hazas et al., 2018 | Neuroblastoma SH-SY5Y and neuronal-like LUHMES cells | HT, HT acetate, HT sulphate, HT acetate-sulphate | 2.5–10 μM | Neuroprotection after oxidative injury observed after the pre-incubation with HT acetate. | [20] |
| Gallardo-Fernández et al., 2019 | Murine microglial BV2 cells | HT | 1–50 µM | Inhibition of α-synuclein aggregation and of NF-ĸB activation. | [34] |
| Leri et al., 2019 | SH-SY5Y cells treated with Aβ1-42 oligomers | HT and oleuropein | 0–20 µM | HT in synergy with oleuropein activated the autophagic flux to prevent cell damage. HT alone accelerated the formation of harmless fibrils while reducing harmful ones. | [35] |
| Hsu et al., 2021 | Human cortical neuronal HCN-2 cells treated with rotenone | HT | 30 μM | Inhibition of rotenone-induced cytotoxic responses by limiting Ca2+ entry. HT reversed ROS levels, cytotoxic responses, and antioxidant enzyme activities (SOD, GPX, and CAT) in rotenone-treated cells. | [36] |
| Mursaleen et al., 2021 | hCMEC/D3-SH-SY5Y cell co-culture treated with rotenone | HT delivered through nanoformulations | 20–200 µM | Encapsulation increased HT-induced protection against rotenone cytotoxicity and oxidative stress. | [37] |
| Visioli et al., 2022 | 7PA2 cell line transfected with cDNA encoding human amyloid precursor protein APP751 | HT | 5 µM | Increase of new mitochondria at 8 h post-HT treatment and increased mitochondrial fusion and ATP concentrations after 24 h of treatment with HT vs. untreated cells. | [38] |
| Nardi et al., 2023 | SH-SY5Y cells treated with 6-OHDA | HT and derivatives esterified and encapsulated in nanoformulations | 0.005–0.1 μM | Antioxidant capacity of the compounds tested. Better efficacy was observed after encapsulation. | [39] |
| Rivero-Pino et al., 2023 | Human peripheral blood mononuclear cells treated with Aβ1-42 oligomers | HT | 41 µM | Down-regulation of pro-inflammatory cytokine gene expression and of neutrophil activation. | [40] |
6-hydroxydopamine (6-OHDA), amyloid β1-42 (Aβ1-42), catalase (CAT), glutamate–cysteine ligase (GCL), glutathione peroxidase (GPX), glutathione-S-transferase (GST), heme-oxygenase-1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO1), nuclear factor erythroid 2–related factor 2 (Nrf2), nuclear factor ĸB (NF-ĸB), reactive oxygen species (ROS), superoxide dismutase (SOD).