Table 2.
In vivo experiments on the anti-neurodegenerative properties of NS or TQ in AD.
| Animal models | Methods | Tests | Results | References |
|---|---|---|---|---|
| Wister-albino rats with ischemia-reperfusion injury (IRI) in hippocampus | TQ (5 mg/kg/day p.o.) 5 days before ischemia and continued during the reperfusion time. | Histological and Histochemical studies | TQ pre-treatment significantly attenuated the loss of hippocampal neuronal cells (P < 0.001), reduced the malondialdehyde's level and increased GSH, catalase and SOD activities. | Al-Majed et al., 2006 |
| Sprague Dawley rats underwent to 2VO surgery | NSO (1 mg/kg), OG daily for 10 days prior to 2VO surgery and then for 70 days post 2VO surgery. | Memory tests | NSO had a protective effect on spatial cognitive functions. | Hosseinzadeh et al., 2007 |
| Wistar rats with IRI | NS (ip 1mg/kg, 10mg/kg and 50 mg/kg), during the carotid clamp and after 72 h. | histopathological examinations | Prevention of intracellular edema of hippocampal interneurons and astrocytes with the highest dose (50 mg/kg). | Hobbenaghi et al., 2014 |
| Wistar rats received IP injection of Aβ-25-35 (1 μl into the CA1 region) or scopolamine (IP 1 mg/kg) | Thymol (0.5, 1, or 2 mg/kg); Carvacrol (0.5, 1, or 2 mg/kg) IP injected 30 min before MWM. | Memory test; Acute toxicity | Thymol and carvacrol improved cognitive functions and reversed the effect of Aβ and scopolamine. | Azzubaidi et al., 2012 |
| Rats with experimentally induced AD (LPS) | TQ (10 mg/kg IP), or nAChR agonist, plus PAM (for 5 days). | Histological and Histochemical studies | TQ, or a α7 nAChR agonist, in combination with PAM, attenuates neuroinflammation and activates MSCs. | Azizi et al., 2012 |
| Streptozotocin-Induced Diabetic Rats | NSO (2 ml/Kg orally), MT (100 mg/Kg), GI (0.8 mg/Kg), and the insulin receptor inhibitor IOMe-AG538 (21 days). | Serum biochemical assays; Neuroinflammation cytokines profile; Brain oxidant and antioxidant markers expression; Cholinergic function; AGEs and brain insulin resistance. Modification of brain AD-related miRNA expression profile, were observed | NSO and the anti-diabetic drugs alone and/or in combination suppressed the oxidative stress, the amyloidogenic pathway and the pro-inflammatory mediator. A reduction in the insulin receptor inhibitory effect of IOMe-AG538 and a modification of the insulin-signaling pathway. | Balbaa et al., 2016, 2017 |
| Rats with memory deficits induced by LPS. | 2, 5, or 10 mg/kg TQ extract 30 min before IP LPS | Behavioral tests (PA, MWM); Biochemical measurements in hippocampal and cortical tissues | TQ was able to enhance memory impairments by reducing the hippocampal cytokine levels and brain's damage. | Bargi et al., 2017 |
| Sprague Dawley rats fed with a high fat-cholesterol diet | TQ rich-fraction nanoemulsion (TQRFNE); TQ emulsion; TQ nanoemulsion. | Memory test (MWM); Serum antioxidant status; Genes expression levels in brain cortex and hippocampus | TQRFNE ameliorated behavioral changes, lipid peroxidation and soluble Aβ levels. Improved radical scavenging activity and increased antioxidants genes expression levels. | Ismail et al., 2017 |
2VO, bilateral carotid arteries occlusion; NSO, Nigella Sativa oil; OG, oral gavage; IIP, intrahppocampal injection; IP, intraperitoneal injection; MWM, Morris water maze; AD, Alzheimer's Disease; Ischemia-reperfusion injury (IRI); TBRAS, thiobarbituric acid reactive substances; MDA, malondialdehyde; LPS, lipopolysaccharide; MSCs, mesenchymal stem cells; PAM, positive allosteric modulator (of nAChR); MT, Metformin; GI, glimepiride; TNF-α, tumor necrosis factor-α; MT, metformin; GI, glimepiride; AGEs, advanced glycation end products; PA, passive avoidance test; TQRFNE, TQ rich-fraction nanoemulsion.