# Protective Effects of _Allium sensecens_ Extract against 6-Hydroxydopamine in Neurons
## 1 Introduction  
Neurodegenerative disorders are caused by oxidative stresses, the dysfunction of mitochondria, and misfolded proteins [1, 2]. These disorders are enhanced by exposure to specific chemicals including 6-OHDA, 1-methyl-4-phenyl tetrahydropyridine (MPTP), annoarcin, and antagonistic compounds to \(\beta\)2-adrenooreceptor [3, 4, 5]. Oxidative inflammation is a common feature of chronic neurodegenerative pathologies in the central nervous system (CNS) [6]. In neurodegenerative disorders, various antioxidants in phytoextracts are effective in preventing the disorders without side effects [7]. Additionally, the activation of various compounds, including levodopa, dopamine agonists, safinamide, and monoamine oxidase B (MAO-B) inhibitors has been used to treat the disorders [8, 9]. SH-SYSY cells and neuroblastoma cells are used widely in various neuronal studies for metabolism, neurotoxicity, neuroprotection, and differentiation. Among these, this cell line is the most applied for neurodegenerative disorders [7, 10]. In neurodegenerative studies, cell lines exposed to 6-hydroxydopamine (6-OHDA) are commonly utilized [11]. 6-OHDA, a neurotoxin, is known to induce neurodegenerative disorders besides PD [12]. Although 6-OHDA does not induce all neurodegenerative disorders, 6-OHDA exposure models in neurons have presented various pathologic features, including neurodegeneration, inflammation, and apoptosis due to oxidative stress [12]. 6-OHDA enters dopaminergic and noradrenergic neurons and inhibits the reuptake of their neurotransmitters [13]. During neuronal destruction, reactive oxygen species (ROS), such as superoxide, accumulate in neurons [14]. Underintrinsic cellular stresses, such as DNA damage, hypoxia, UV, and exposure to chemicals, mitochondria in neurons release cytochrome c through assembled Bax proteins, and the released cytochromes and activated caspase 9 enhance cellular apoptosis [15]. When 6-OHDA triggers the production of ROS, monoamine oxidase (MAO) A and B are expressed in the neurons, and MAOB produces ROS through the degradation of dopamine in neurons [16]. To protect against stress, cells express several proteins, including members of the B-cell leukemia/lymphoma 2 (Bcl-2) family [17], cytokine response modifier A (crmA) [18], and inhibitors of apoptosis proteins (IAPs) [19]. The Bcl-2 family of 20 proteins is involved in the regulation of cellular apoptosis. The Bcl-2 proteins (A1, Bcl-2, Bcl-w, Bcl-xL, Bcl-B, and Mcl-1; myeloid cell leukemia sequence 1) inhibit apoptotic proteins, including Bax, Bak, and Bok [20]. Caspase-3 (Cas3) interacts with caspase-8 and -9, which play a central role in apoptosis, and Cas3 activates the production of the A\(\beta\) peptide from the cleavage of the amyloid-beta 4A precursor protein associated with [PERSON]'s disease [21].  
_Allium senescens_ is a perennial aromatic herb distributed in northern Europe and Asia, especially on Ulleung Island in Republic of Korea [22]. _A. senescens_ is effective in refreshing blood and controlling cholesterol levels in the blood [23] to activate detoxification and restore functions in the liver [24]. Based on the reported chemical compositions [25], _A. senescens_ extract contains various bioactive compounds, including allin, allicin, ocular acid, ferulic acid, and isoquercitrin.