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Neuroprotective Potential of Secondary Metabolites From Melicope lunu-ankenda (Rutaceae)

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Review

Neuroprotective Potential of Secondary Metabolites From Melicope lunu-ankenda (Rutaceae)

Zeinab Abdulwanis Mohamed et al. Molecules.

Abstract

Plant natural compounds have great potential as alternative medicines for preventing and treating diseases. Melicope lunu-ankenda is one Melicope species (family Rutaceae), which is widely used in traditional medicine, consumed as a salad and a food seasoning. Consumption of different parts of this plant has been reported to exert different biological activities such as antioxidant and anti-inflammatory qualities, resulting in a protective effect against several health disorders including neurodegenerative diseases. Various secondary metabolites such as phenolic acid derivatives, flavonoids, coumarins and alkaloids, isolated from the M. lunu-ankenda plant, were demonstrated to have neuroprotective activities and also exert many other beneficial biological effects. A number of studies have revealed different neuroprotective mechanisms for these secondary metabolites. This review summarizes the most significant and recent studies for neuroprotective activity of M. lunu-ankenda major secondary metabolites in neurodegenerative diseases.

Keywords: Melicope lunu-ankenda; alkaloids; coumarins; neurodegenerative diseases; neuroprotection; polyphenols.

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
General chemical structure of hydroxycinnamic acid. Adapted from Soobrattee et al. [8].
Figure 2
Figure 2
General chemical structure of hydroxybenzoic acid. Adapted from Soobrattee et al. [8].
Figure 3
Figure 3
General chemical structure of flavonoids. Adapted from Soobrattee et al. [8].
Figure 4
Figure 4
The mechanisms of neuroprotective activity exhibited by polyphenols. ARE, antioxidant response element; GSH, glutathione; ROS, reactive oxygen species; Nrf2, nuclear factor (erythroid-derived 2)-like 2; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; iNOS, inducible nitric oxide synthase; HO-1, heme oxygenase 1; Sesn2, sestrin 2; GCL, glutamate-cysteine ligase; GSTs, glutathione S-transferase; Keap1, Kelch-like ECH-associated protein 1; sMAF, proto-oncogene response element; SOD, superoxide dismutase; IL, interleukin; IFN-γ, interferon-gamma; GPx, glutathione peroxidase; TNF-α, tumor necrosis factor-alpha; TGF-β, transforming growth factors β; COX-2, cyclooxygenase-2; MCP-1, monocyte chemoattractant protein-1; SIRT-1, silent mating type information regulation 2 homolog 1; JNK, c-Jun N-terminal kinase; Bcl-2, B-cell lymphoma-2; Bad, BCL2-associated agonist of cell death; BAX, BCL2-associated X protein; Aβ, amyloid beta; AChE: acetylcholinesterase; ERK, extracellular signal-regulated kinase; PKC, protein kinase C; PI3K, phosphatidylinositol 3-kinase; Akt, protein kinase B; PPAR, peroxisome proliferator-activated receptor; CXCL10, chemokine (C-X-C motif) ligand 10; CCL, chemokine (C-C motif) ligand; CCR, chemokine receptor; MIP1α, macrophage inflammatory protein 1 α; MAPKs, mitogen-activated protein kinases; CI, cerebral ischemia; cysDA, cysteinyldopamine; MDA, malondialdehyde; Ub, Ubiquitin.
Figure 5
Figure 5
General chemical structure of coumarins. Adapted from Jameel et al. [50].
Figure 6
Figure 6
The mechanisms of neuroprotective activity exhibited by auraptene. COX-2, cyclooxygenase-2; iNOS, inducible nitric oxide synthase; TNF-α, tumor necrosis factor-alpha; GSH, glutathione; SOD, superoxide dismutase; MDA, malondialdehyde; PGE2, prostaglandin E2; CREB, cAMP response element-binding protein; ERK1/2, extracellular signal-regulated kinase 1 or 2.
Figure 7
Figure 7
General chemical structure of furoquinoline alkaloids. Adapted from Wansi et al. [65].
Figure 8
Figure 8
General chemical structure of chromenes. Adapted from Johnson et al. [5].

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