## 4 Discussion
Additionally, Z increased skin hydration content compared with the UVB-irradiated control group. Moisture content plays an important role in all aspects of skin aging. Recently, _Ullica thuntergiana_ also increased skin moisture content in the background of UVB-irradiation in an in vivo study [43]. In living cells, UV irradiation regulates nuclear factor-kappa B (NF-kB) expression by activating mitogen-activated protein kinase (MAPK) and generating ROS [44]. The MAPK pathways regulate the transcription factor activating protein 1 (AP-1), a heterodimer consisting of c-Fos and c-Jun, thereby upregulating MMPs in the skin [45; 46]. Z reduced the mRNA or protein expression of MAPK, AP-1, MMP1, MMP3, and MMP-9 compared to the UVB-irradiated control group. Moreover, Z increased the mRNA or protein expression of procollagen and collagen type 1 compared to the UVB-irradiated control group. More than 90% of collagen, which is the most abundant in the dermis, exists in the form of collagen type I produced from procollagen [47]. Among the MMPs, MMP-3 has a substrate specificity for collagen type IV, and MMP-2 has substrate specificity for collagen type IV as well as gelatin. MMP-2 and MMP-9 are known as gelatinases A and B, but MMP-3 acts as a promotor for MMP-1 and MMP-9. As MMP-1 activity leads to MMP-9 activity through MMP-2 activity, it is pertinent to identify MMP-1, MMP-3, and MMP-9 in this study [48]. UVB stimulates ROS production after reaching the skin epidermis, causing oxidative damage to cell membrane lipids and promoting the release of proinflammatory cytokines such as IL-1\(\beta\), IL-6, and TNF-\(\alpha\)[2; 49]. These inflammatory reactions can cause skin disease such as psoriasis, wrinkles and atopic dermatitis [50]. In addition, they are known to increase the expression of MMPs, reduce collagen synthesis, promote degradation, reduce skin elasticity, and promote skin aging [51]. Z reduced the mRNA expression of IL-1\(\beta\), IL-6, and TNF-\(\alpha\) compared to that in the UVB-irradiated control group, and increased the activities of SOD, catalase, and GPx compared to that in the UVB-irradiated control group. Oxidative stress is caused by overloading free radicals or insufficient antioxidants and increases during exposure to infection from contaminants, inflammation, sunlight and radiation. These oxygen radicals damage cellular DNA and proteins, causing a variety of cancers, including skin cancer. Some phytochemicals have been shown to maintain the homeostasis of the redox state of intracellular enzymes [52; 53; 54; 55]. Melanin has important physiological functions such as protecting skin from UV damage by absorbing UV light and removing ROS [56]. However, excessive melanin production can lead to pigmentation, post-inflammatory hyper pigmentation, solar lentigo, and melanoma. To prevent these stresses, tyrosinase inhibitors and melanogenesis inhibitors have been developed [57; 58]. Melanin pigments are synthesized as either red based eumelanine or brown based pheomelanin, which begins with the activation of tyrosine in melanocytes. In addition, the amount of L-tyrosine and L-DOPA increases, leading to the increase in the levels of tyrosinase-related protein 2 (TRP-2) and TRP-1 through the synthesis of L-dopaquinone [59; 60; 61]. The expression of tyrosinase and TRP-1 gene is activated by MITF, which is activated by cyclic adenosine monophosphate (cAMP). Thus, the down-regulation of melanocyte migration in melanocytes leads to the mechanism of depigmentation and down-regulation of melanin synthesis [62; 63]. Z reduced the mRNA or protein expressions of CREB, MITF, tyrosinase, and TRP-1 compared to the UVB-irradiated control group. These results are in line with the recent findings that Bamboo stems or the flower extracts from _Paeonia decomposita_ and _Paeonia ostii_ inhibit melanogenesis through the CREB-mediated pathway [64; 65].