## 1 Introduction  
The hair follicle is a complex structure made up of epithelial (the matrix, the inner root sheath (IRS), and the outer root sheath (ORS) and dermal (the dermis) components (dermal papilla and connective tissue sheaths) [1]. The hair bulb is the primary structure at the base of the hair follicle, where the oval and indented dermal papilla (DP) is found. It contains blood vessels that deliver nutrients and energy necessary for hair growth [2]. In addition to being programmed for cyclical regeneration, hair follicles undergo a growth phase (anagen), a regression phase (catagen), and a relatively quiescent phase (telogen) [3]. When high levels of reactive oxygen species (ROS) are encountered, the DP is exposed to a stressful environment. Antioxidant systems should be able to efficiently remove these ROS. Oxidative stress in hair follicles has been proposed to be a causative factor in the induction of different disorders that result in hair loss [4]. An oxidant/antioxidant imbalance is a common feature in autoimmune disorders, including alopecia areata (AA) [5]. AA was reported to be induced by a redox imbalance, which is mediated by abnormal T-cells-mediated adaptive immunity [6, 7]. High levels of oxidative stress were reportedto trigger abnormal innate immune responses in AA [8; 9]. As biomarkers for oxidative stress, lipid peroxides and their degradation product malondialdehydedehyde were found to be increased in AA lesions [10; 11; 12]. Antioxidant defense system impairment has been consistently reported to be a causal factor of AA. Superoxide dismutase (SOD) activity has been shown to decrease in serum and erythrocytes of AA patients [9; 12]. Additionally, SOD activity inversely correlates with the severity or duration of AA and was found to be further reduced in the most severe form of AA or AA of longer duration (\(\geq\)6 months) [13]. Glutathione peroxidase, which converts hydrogen peroxide to water and oxygen in the presence of glutathione, is reduced in both scalp tissues and plasma and erythrocytes of patients with AA.tocopherol and \(\beta\)-carotene, which are essential fat-soluble vitamins, function as important protectors of the cell membrane against lipid peroxidation, and they interact preferentially with free radicals, such as lipid peroxyl radicals [14]. Decreased levels of vitamin E and \(\beta\)-carotene in AA tissue or circulating blood have also been reported [10; 15]. In androgenetic alopecia (AGA), the most common form of male baldness, the balding scalp was found to have been exposed to high levels of oxidative stress, which cause the secretion of TGF-\(\beta\), a hair growth inhibitory factor [16]. These studies suggest that oxidative stress in hair follicles is involved in the pathogenesis of hair loss. As a master regulator of redox homeostasis, nuclear factor erythroid 2 (NFE2)-related factor 2 (Nrf2) performs detoxifying and antioxidant activities in the skin [17]. This transcription factor regulates a set of genes that includes heme oxygenase-1 (HO-1), NAD(P)H quinone oxidoreductase-1, SOD, glutathione S-transferase (GST), and glutamate-cysteine ligase, which are involved in the detoxification and antioxidant defense [18]. The group of NRF2-mediated phase II detoxifying and antioxidant (phase II enzymes) comprises of factors essential for maintaining normal cellular integrity in the skin and hair follicles. These follicle cells and the scalp are continually exposed to harmful conditions. Therefore, NRF2-dependent protection from oxidative stress in hair follicles could be essential for their maintenance to ensure normal function and integrity. Dermal papilla cells (DPCs), the major cellular component of DP, play a crucial role in morphogenesis and hair growth cycling. Recently, DPCs have been extensively used in in vitro screening models to evaluate the efficacy of agents tested for their hair growth-modulating activities.