Table 1.
Plant part, extraction methods and biological activities and results.
| Plant Part | Extraction Method/Type | Bioactivity | Model | Main Results | Ref. |
|---|---|---|---|---|---|
| Leaves | Ethanolic extract | Neuroprotective | In vitro: anti-oxidant activity | Dose-dependently (6.25–100 mg/mL) enhanced scavenging activity against ABTS and DPPH radicals | [9] |
| Neuroprotective | In vitro: HT22 neuronal cell death | Extract significantly reversed H2O2-induced neuronal cell death at 25 or 50 µg/mL | [9] | ||
| Neuroprotective | In vivo: Aβ-injected AD like mouse-model | Increased expression of NeuN and BDNF in hippocampus reversing the effects of intracerebroventricular injection of Aβ aggregates | [9] | ||
| Neuroprotective | In vivo: Aβ-injected AD like mouse-model | Reduced the Aβ-mediated phosphorylation of EGFR and GRK2 | [9] | ||
| Anti-Alzheimer’s | In vitro: Aβ aggregation | Dose-dependently inhibited Aβ aggregation by 91.35% at 100 mg/mL | [9] | ||
| Anti-Alzheimer’s | In vivo: Aβ-injected AD like mouse-model | At 100 μg/mL extract significantly attenuated the effects of Aβ aggregation in the passive avoidance task and Y-maze test | [9] | ||
| Neuroprotective | In vivo: SCO-induced hippocampal neuronal damage | Prevented scopolamine-induced neuron damage in SCO-mediated memory deficit mice as shown by cresyl violet staining | [11] | ||
| Neuroprotective | In vivo: cholinergic function in scopolamine-treated Mice | Increased acetylcholine content, choline acetyltransferase, and acetylcholinesterase activity in the hippocampus of SCO-treated mice | [11] | ||
| Neuroprotective | In vivo: oxidative Stress in scopolamine-treated Mice | Attenuated the SCO-induced increase in reactive oxygen species (ROS) levels in the hippocampus | [11] | ||
| Neuroprotective | In vivo: neuronal apoptosis in SCO-treated mice | Significantly decreased apoptotic activation in hippocampus of SCO-treated mice | [11] | ||
| Anti-Alzheimer’s | In vivo: SCO-induced cognitive deficit mouse model | Significantly attenuated the memory deficits from scopolamine treatment in passive avoidance task and Y-maze test | [11] | ||
| Antioxidant | In vitro: ABTS and DPPH free radical scavenging assays | At 100 μg/mL, AALE dose-dependently enhanced scavenging activity against ABTS and DPPH radicals by 97% and 82% respectively. | [11] | ||
| Antioxidant | In vitro: ABTS, DPPH and FRAP free radical scavenging assays | ABTS 5.01 TE g−1 DPPH 13.51 TE g−1 14.79 TE g−1 |
[31] | ||
| Anticancer | In vitro: cytotoxicity HeLa, HepG2 cells | GI50 ~ 2 µg/mL | [31] | ||
| Antinociceptive activity | In vivo: acetic acid-induced writhing and formalin mouse models | AAIW 100 mg/kg inhibited writhing 63.48% FMM 100 mg/kg inhibited pain response 63.48% |
[45] | ||
| Anti-inflammatory | In vivo: air pouch mouse model In vivo: carrageenan-induced peritonitis mouse models |
100 mg/kg inhibited leukocyte migration in to air-pouch by 73.16% 100 mg/kg inhibited leukocyte migration by 63.85% |
[45] | ||
| Methanolic extract | Antibacterial | In vitro: against strains of S. epidermidis, B. cereus, methicillin-resistant S. aureus, K. pneumoniae and S. aureus. | MBC range 3125 to 12,500 µg/mL. | [46] | |
| Hexane extract | Antioxidant | In vitro: inhibition of β-carotene-linoleic acid bleaching assay | 41.12 ± 4.35% inhibition | [46] | |
| Seeds | Ethanolic extract | Anti-angiogenic | In vitro and in vivo models, involving cell proliferation, HUVEC and tumour-induced angiogenesis. |
EEAA dose-dependently inhibited HUVEC proliferation at conc. ≥ 100 μg/mL. | [12] |
| Anticancer | In vitro: cytotoxicity Hep G2, Hep 2,2,15, KB, CCM2 and CEM cells | Isolated acetogenins ED50 from 2.2 × 10−4 to > 500 µg/mL | [20,44] | ||
| Neurotoxicity | In vitro: LUHMES cells | 0.1 µg/mL reduced cell viability to 4.0% ± 0.8% | [50] | ||
| Methanolic | Antioxidant | ABTS and DPPH free radical scavenging assays | 46.14 ± 1.25 and 4.82 ± 0.32 μmol TE g−1 | [47] | |
| Larvicidal | In vitro: Trichoplusia ni | Topical LC50 197.7 µg/larva Oral LC50 382.4 ppm |
[51] | ||
| Stem | Ethanolic extract | Antioxidant | In vitro: ABTS and DPPH free radical scavenging assays | DPPH; IC50 = 10.44 ± 1.25 µg/mL ABTS; IC50 = 24.81 ± 0.49% |
[46] |
| Antibacterial | In vitro: against S. epidermidis, B. cereus, methicillin-resistant S. aureus, K. pneumoniae, S. aureus. | MBC range 781–6250 µg/mL. | [46] | ||
| Fruits | Ethanolic extract | Hypolipidemic Effect | In vivo: oral administration of extracts to Female KKAy mice (5 weeks of age) fed a high fat diet for 4 weeks | Significantly lowered the plasma triglyceride (TG) concentration at doses of 125 and 500 mg/kg. | [48] |
| Ethanolic and hexane extracts | Anti-Obesity Activity | In vitro: 3T3-L1 cell line | 50% or more inhibition of adipogenesis in 3T3-L1 cells. | [49] | |
| Ethanolic extract | Neurotoxicity | In vitro: LUHMES cells | 10 µg/mL decreased cell viability to 12.7% ± 3.7% | [50] |
AAIW acetic acid induced writing; Aβ β-amyloid; ABTS 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid; AD Alzheimer’s disease; AALE A. atemoya leaf extract; BDNF brain derived neurotropic factor; DPPH 2,2-diphenyl-1-picrylhydrazyl; EEAA ethanol extract A. atemoya; EGFR epidermal growth factor receptor; FMM formalin mouse model; FRAP ferric reducing antioxidant power; GRK2 G protein-coupled receptor kinase 2; HUVEC: human umbilical vascular endothelial cells; MBC minimum bactericidal concentration; NeuN neuronal nuclear protein; ROS reactive oxygen species; SCO scopolamine.