Purpose: The active melanocytes in the skin were affected by hormones and ultraviolet (UV) irradiation. Licorice zinc has a whitening effect, which may have a prominent potential in the treatment of pigmented skin disease. Methods: Modeling chloasma C57BL/6J mice by daily progesterone injection (15 mg/kg) and ultraviolet B (UVB) irradiation (λ = 312 nm, 2 h/day) for 30 days. Then, mice were given 0.65, 1.3, and 2.6 (g/kg) of licorice zinc and tranexamic acid 250 mg daily by oral administration for 14 days, respectively. Hematoxylin and eosin and Fontana-Masson staining, and Western blotting (WB) were performed to test the inhibitory of melanogenesis and activation of c-Jun-N-terminal (JNK)/p38 mitogen-activated protein kinases (MAPK) for licorice zinc. Melanogenesis was induced by α-melanocyte-stimulating hormone in vitro . Cell counting kit-8, melanin content determination, and WB were performed to verify the inhibitory effect of licorice zinc on melanogenesis. Results: The present study showed that licorice zinc decreased melanin formation, cutaneous tissue injury, and the phosphorylation of JNK and P38MAPK, which was caused by UVB irradiation in vivo . In vitro , licorice zinc showed opposite effects from JNK/p38 activator. Meanwhile, tyrosinase-related protein-1, tyrosinase, and microphthalmia-associated transcription factor were decreased too. Conclusions: Licorice zinc induced a decrease in melanin synthesis by inhibiting the JNK and the P38MAPK signaling pathway, suggesting licorice zinc is a potential agent of anti-chloasma.

Black rot disease is a serious bacterial disease that harms vegetable crops of the Brassica genus (especially cabbage plants) worldwide. The causal agent, Xanthomonas campestris pv. campestris (Xcc), is a seed-borne pathogen that primarily infects seedlings. Previous studies suggest that the bacterial strain, Bacillus amyloliquefaciens PMB05, can intensify the plant immune responses of cabbage against black rot disease and reduce disease occurrence. In plant immunity, several reactions occur during a pathogen attack, but the elevation of calcium ion concentration in plant cells is essential in the induction of plant defense responses. Therefore, this study aims to investigate whether disease control of black rot disease in cabbage plants can be improved by integrating calcium carbonate in the formulation for preparing B. amyloliquefaciens PMB05. Firstly, we found the addition of calcium carbonate in the formulation revealed to have significantly increased the cell and endospore populations of B. amyloliquefaciens PMB05 in the fermentation liquids. To increase the convenience of disease control in the field, these fermentation liquids were converted to powder form for subsequent analysis. Results revealed that the grown seedlings from seeds, mixed with PMB05 powders, significantly intensified plant immune responses and improved black rot disease control. We further compared distinct seed treatments using one PMB05 powder to evaluate its feasibility in field application. The results demonstrated that the disease control efficacy and yield of cabbage were significantly improved in the seed treatment with the powder (SD-160C2) to 56.46% and 5.91%, respectively, at 10 weeks post transplanting. Interestingly, the seed treatment combined with a calcium-containing commercial fertilizer spraying treatment did not increase the control efficacy of black rot disease, but it significantly increased the weight of cabbages after harvest. We concluded that the seed treatment with calcium carbonate-containing Bacillus amyloliquefaciens PMB05 powder is an efficient way to control black rot disease in cabbage.

In order to prove that SOX9 in keratinocytes regulates claudin 2 transcription during skin aging, the skin of 8-week-old and 24-month-old mice is sequenced to obtain a differentially expressed gene SOX9. The gene is mainly expressed in keratinocytes, and it increases first and then decreases from newborn to aging. Six core sequences of SOX9 and claudin 2 are predicted from Jaspar. The double Luciferase Report shows that overexpression of SOX9 induces the full-length promoter of claudin 2 significantly and has no effect on the mutation and cleavage plasmid without SOX9 response. Claudin 2 is consistent with SOX9 in the skin of mice of different ages, and SOX9 is strongly positively correlated with claudin 2. Finally, overexpression of SOX9 and claudin 2 will delay PM2.5-induced keratinocyte senescence. The silencing of claudin 2 leads to the loss of SOX9 function. It is clearly evident that SOX9 can affect the transcription of claudin 2, which increases first and then decreases in the process of mice from newborn to aging. SOX9 inhibits proinflammatory mediators, increases antioxidant capacity, and restores keratin differentiation. It can effectively prevent melanin deposition and delay aging.