## 4 Discussion  
Ginsenosides are the primary bioactive compounds found in ginseng. However, because ginsengosides are mostly in glycoside form, they are not entirely absorbed by the body [43; 44; 45]. To overcome this limitation, ginseng can be fermented with bio-transforming microorganisms to convert the existing saponins into saponin metabolies ingested in the body [35]. In a previous study, we discovered that _Aspergillus niger_ KHNT-1 proficiently converts the ginseng Rb1 by \(\beta\)-glucosidase hydrolysis into the primary active constituent, which is not present in WG. FBG contained a substantial amount of CK, Rg3, Rg5, and Rk1, with contents of 38.13, 19,926.07, 15,217.9, and 9193.77 mg/kg DW, respectively [29]. Apart from ginseng, phenolic and flavonoid compounds are also found in ginseng; these compounds are well known to have antioxidant and anticancer activities. Among the phenolic compounds found in ginseng are gallic acid, vanillic acid, p-hydroxybenzoic acid, gentisic acid, caffeic acid, ferulic acid, and p-coumaric acid [20]. In the present study, FBG phenolic and flavonoid contents were significantly higher than BG and WG (Table 3). Previous studies also reported that TPC and TFC are increased by fermentation [46; 47]. Along with an increase in TPC and TFC, as well as the biotransformation of ginsengosides, the antioxidant activities in DPPH and reducing power assays were increased, indicating that FBG has a better antioxidant effect than BG and WG. Skin aging has remained a critical dermatologic concern in society, and theoretical concepts have been proposed to investigate the cause and effects. Excessive melanin biosynthesis causes hyperpigmentation, leading to various dermatological conditions such as freckles, age  
Figure 5: The antioxidant effects of FBG, BG, and WG on H\({}_{2}\)O\({}_{2}\)-induced ROS levels in HaCat cells. (**A**) Cytotoxicity effect of FBG, BG, and WG in HaCat cells for 24 h. The cytotoxicity effect was then determined with MTT assays. (**B**) HaCat cells were treated with FBG, BG, or WG (100 \(\upmu\)g/mL) for 24 h before exposure to H\({}_{2}\)O\({}_{2}\) (500 \(\upmu\)M) for 2 h. ROS level was detected by DCFH-DA and examined with a 10x fluorescence microscope. Scale bar: 100 \(\upmu\)M. (**C**) Intracellular ROS level (% of control). The graph shows mean \(\pm\) SD values of four replicates. ## \(p<0.01\), as compared with the control group; *\(p<0.05\), **\(p<0.01\), as compared with the H\({}_{2}\)O\({}_{2}\) stimulation group. spots, melasma, and even skin cancer. Hyperpigmentation, wrinkles, and sagging skin are all signs of skin aging [48]. Various intracellular and extracellular stimuli, including UV light and chemicals such as \(\alpha\)-MSH and IBMX can stimulate melanogenesis [49; 50; 51]. IBMX can increase cellular cAMP levels by inhibiting phosphodiesteraseerase, this response activates the PKA signaling pathway, which regulates MITF as a transcription factor and element-binding protein of cAMP-responsive; this process is involved in the regulation of melanogenic vital enzymes such as tyrosinase, TRYP-1, and TYP-2 [49; 52]. Tyrosine is the primary target for melanin inhibition. Therefore, tyrosinase inhibitors are found in most commercial cosmetics and skin-lightening agents [53; 54; 55; 56]. FBG inhibited MITF, tyrosinase, and TYP-1 mRNA expression but did not regulate TYP-2 (Figure 2). Consequently, these results suggest that the anti-melanogenic effect of FBG is not directly affected by tyrosinase activity but through downregulated MITF levels (cAMP signaling pathway). UVB radiation can up-regulate activator protein (AP-1) and stimulate the expression of MMPs, induce inflammation, and activate dermal enzymes such as collagenase and elastase. Excessive levels of these enzymes can degrade collagen and elastain, causing premature skin aging [57]. Aside from collagen degradation in the skin, increased elastase levels trigger the loss of the skin's elasticity and internal structure [58].