Table 1.
In vitro studies on the effects of NS or TQ in AD.
| Cell lines/in vitro test | Drugs and dosages | Main results | References |
|---|---|---|---|
| Dried plant /AChE inhibition assay | Galanthamine; Thymohydro-quinone Carvacrol; Thymol; Linalool. (10-0,00001 mg/mL) | AChE inhibitory potential decreased as follows: Galanthamine > Thymohydro-quinone > Carvacrol > TQ > Total essential oil > Thymol > Linalool. | Jukic et al., 2007 |
| Primary rat CGNs | NSO (500–2 mg/mL) | NSO and its fractions prevented the Aβ toxicity (NSO, and WF more than HF, and EAFs). | Ismail et al., 2008 |
| PC-12 | TQ (0.78–400 μM) | TQ: (1) ameliorated induced loss of cell viability; (2) prevented the Aß25–35-induced increase activity of LDH; (3) had protective effects on GPx, GR, and AChE in PC 12 cells exposed to Aß25–35; (4) downregulated the iNOS expression along with NO level; (5) had a protective role of intracellular oxidative stress, by restoring the ROS level; (6) augmented the membrane potential by restoring the normal level of MMPs. | Khan et al., 2012 |
| E18 | TQ (0.1, 1, 10, 100 nM) | TQ: (1) reduced intracellular ROS level in neurons treated with Aß1–42; (2) reduced Aß-induced inhibition of synaptic vesicle recycling. | Alhebshi et al., 2013 |
| CGNs | TQ (0.1 and 1 μM) | TQ had protective effects on Aß1–40-induced neurotoxicity by reducing the production of free radical on Aβ1–40 in CGNs and by attenuating the activation of Caspase-3,−8, and−9 on Aß1–40 exposure. | Ismail et al., 2013 |
| Rat primary hippocampal cells; hiPSC-derived neurons | TQ (100 nM) | TQ: (1) neurons were protected against SN-induced synapse damage and the synaptophysin was enhanced; (2) maintained the synaptic activities in hippocampal neurons were maintained; (3) the uptake of FM1-43 dye increased, while the inhibitory effect of SN on synaptic vesicle recycling was decreased. | Alhebshi et al., 2014 |
| SH-SY5Y | TQ, EGCG; DLPC | TQ prevented the oxidation of Aß by decreasing the expression of NO and by increasing the GSH levels. | Kennedy et al., 2014 |
| BV-2 | TQ (0–40 μM) | TQ treatment in the LPS/IFNγ-activated microglia altered the expression profiles of Ccl5, Nos and Ptgs2. | Cobourne-Duval et al., 2016 |
| N2a | NOS encapsulated in Nanoparticles-pDNA (ratio from 5 to 50%) | Encapsulated NSO promoted neurite outgrowth of N2a cells. | Doolaanea et al., 2016 |
AChE, acetylcholinesterase; NSO, Nigella Sativa Oil; TQ, Thymoquinone; CGNs, cerebellar granule neurons; HF, hexane fraction; EAF, ethyl acetate fraction; WF, water fraction; GPx, glutathione peroxidase; GR, glutathione reductase; Aß, amyloid beta; iNOS, Inducible nitric oxide synthase; NOS, nitric oxide synthase; ROS, Reactive oxygen species; MMPs, Matrix metalloproteinases; ß-amyloid peptide 1–40 sequence, Aβ1–4; human induced pluripotent stem cells (hiPSC); α-synuclein, αSN; (FM1-43 dye, N-(3-Triethylammoniumpropyl)-4-(4-(Dibutylamino) Styryl) Pyridinium Dibromide); NO, nitrix oxide; GSH, glutathione; LPS, lipopolysaccaride; IFNγ, Interferon-gamma; Ccl5, Chemokine (C-C) motif ligand; Nos2, nitric oxide synthase 2 inducible; Ptgs2, Pros-taglandin-endoperoxide synthase 2; Txnip, Thioredoxin-interacting protein; Prdx 1, Peroxiredoxin 1; S. cerevisiae, Sulfiredoxin 1 homolog.