## 1 Introduction  
The different forms of ultraviolet (UV) radiation, namely, UVA, UVB, and UVC, have varying impacts on the skin depending on their wavelength. Among them, UVB has the most biological activity and is most absorbed by DNA, so it is often considered the main factor behind UV-induced diseases [1, 2]. It mainly acts on the epidermis and extracellular matrix (ECM) by interacting with chromophores and photosensitizers [3, 4].  
Reactive oxygen species (ROS) produced in excess due to UVB irradiation are the primary mediators behind the activation of various oxidative stress pathways [5]. Excessive ROS causes oxidative damage to crucial biomacromolecules (e.g., proteins, lipids, and nucleic acids) in cells and induces mitochondrial DNA damage, apoptosis, and cell cycle arrest [6, 7]. They further upregulate matrix metalloproteinases (MMPs) through pathways such as mitogen-activated protein kinase (MAPK)/activator protein 1 (AP-1) and decompose the ECM, which decreases the strength and elasticity of the skin [8]. Deep wrinkles, inelasticity, and non-healing ulcers caused by the degradation of elastin and collagen fibers in the ECM are the most intuitive manifestations of skin photoaging.  
Many studies have shown that plant supplements can cut oxidative free radicals from hemoglobin and regulate collagen production by upregulating the nuclear erythroid 2-related factor \((\text{Nrf2})/\text{antioxidant}\) response element (ARE) natural antioxidant pathway and the transforming growth factor (TGF)-\(\beta\)/Smad collagen synthesis pathway [9; 10]. Nrf2 is transferred from the cytosol to the nucleus to activate ARE-dependent genes and promote the production of antioxidant enzymes such as NAD(P)H quinone oxidoreductase-1 (NQO1), dihydroamide dehydrogenase (DLD), and heme oxygenase-1 (HO-1) to remove harmful quinones and relieve oxidative stress [11]. The expression of TGF-\(\beta\) is mediated by the Smad protein family [12]. Inhibitory Smads (Smad6 and Smad7) can bind to TGF-\(\beta\) receptors [13] and impede the ability of R-Smad (Smad2 and Smad3) to interact with TGF-\(\beta\) receptors to block the expression of procollagen genes [14]. In this way, the damaged cell structure and function caused by high ROS can be restored to achieve anti-photoaging effects.  
Jawoongo (JAUN) is a traditional ointment commonly used in China, Japan, and Korea for inflammatory diseases of the skin, dry and keratinizing diseases, burns, trauma, abnormal pigmentation, and the prevention and healing of wounds. It is primarily composed of _Lithospermum erythrorhizon_ and _Angelica gigas_, with addition and reduction. The _Lithospermum erythrorhizon_-derived active components of JAUN include naphthoquinone compounds, such as shikonin derivatives, which have been demonstrated to have anti-inflammatory, antibacterial, and antitumor effects, as well as being able to scavenge ROS [15; 16]. In terms of the _Angelica gigas_-derived active ingredients, these include decursin, decursinol angelate, and nodakenin, which have been reported to have therapeutic effects against allergy-related inflammation, as well as anti-cancer and anti-depression activities [17; 18]. The pharmacological properties of JAUN have been substantiated through in vitro and in vivo experiments regarding its ability to prevent atopic dermatitis and promote wound healing [19; 20]. Nevertheless, to the best of our knowledge, no reports on the anti-photoaging properties of JAUN have been published.  
This study was implemented to investigate the activity and mechanisms of action of the JAUN-modified formula on HaCaT cells induced by UVB photoaging. In addition, the anti-photoaging effects of JAUN were investigated by analyzing the levels of MMPs, ROS, and procollagen type I as well as the expression levels of the TGF-\(\beta\)/Smad and Nrf2/ARE signaling pathways, which are key regulatory biomarkers of skin photoaging.