FORMULATION OF SUNSCREEN CREAM OF PARIJOTO FRUIT EXTRACT (Medinilla speciosa Blume) AND IN VITRO SPF VALUE TEST

Sunscreen preparations are cosmetic preparations used as a protection to reduce the impact of sun exposure whose formulations contain active ingredients to absorb or diffuse sunlight, especially in areas of ultraviolet and infrared wave emissions. One of the potential natural ingredients for a sunscreen is parijoto fruit (Medinilla speciosa Blume). It contains flavonoid compounds that are able to prevent the harmful effects of UV rays. The objective of this research is to find out the formula of sunscreen cream of parijoto extract that meets the good physical quality of cream and to find out the result of SPF value test of parijoto fruit extract as sunscreen cream preparation in Vitro. The design of the study was experimental research conducted in the laboratory. The sample used in this research was parijoto made into thick extract by maceration method. Further, the viscous extract obtained was made to be a sunscreen cream and then tested either its physical evaluation or calculation of SPF value. The results of this study indicate that the preparation of sunscreen cream of parijoto fruit extract included in the extra protection category with the value is 6.66 and can be made into the good and stable preparations. The sunscreen cream of parijoto fruit extract has good physical properties and also has activity as UV protection in vitro

FORMULATION OF SUNSCREEN CREAM OF PARIJOTO FRUIT EXTRACT (Medinilla speciosa Blume) AND IN VITRO SPF VALUE TEST

Sunscreen preparations are cosmetic preparations used as a protection to reduce the impact of sun exposure whose formulations contain active ingredients to absorb or diffuse sunlight, especially in areas of ultraviolet and infrared wave emissions. One of the potential natural ingredients for a sunscreen is parijoto fruit (Medinilla speciosa Blume). It contains flavonoid compounds that are able to prevent the harmful effects of UV rays. The objective of this research is to find out the formula of sunscreen cream of parijoto extract that meets the good physical quality of cream and to find out the result of SPF value test of parijoto fruit extract as sunscreen cream preparation in Vitro. The design of the study was experimental research conducted in the laboratory. The sample used in this research was parijoto made into thick extract by maceration method. Further, the viscous extract obtained was made to be a sunscreen cream and then tested either its physical evaluation or calculation of SPF value. The results of this study indicate that the preparation of sunscreen cream of parijoto fruit extract included in the extra protection category with the value is 6.66 and can be made into the good and stable preparations. The sunscreen cream of parijoto fruit extract has good physical properties and also has activity as UV protection in vitro

NDAT Targets PI3K-Mediated PD-L1 Upregulation to Reduce Proliferation in Gefitinib-Resistant Colorectal Cancer

The property of drug-resistance may attenuate clinical therapy in cancer cells, such as chemoresistance to gefitinib in colon cancer cells. In previous studies, overexpression of PD-L1 causes proliferation and metastasis in cancer cells; therefore, the PD-L1 pathway allows tumor cells to exert an adaptive resistance mechanism in vivo. Nano-diamino-tetrac (NDAT) has been shown to enhance the anti-proliferative effect induced by first-line chemotherapy in various types of cancer, including colorectal cancer (CRC). In this work, we attempted to explore whether NDAT could enhance the anti-proliferative effect of gefitinib in CRC and clarified the mechanism of their interaction. The MTT assay was utilized to detect a reduction in cell proliferation in four primary culture tumor cells treated with gefitinib or NDAT. The gene expression of PD-L1 and other tumor growth-related molecules were quantified by quantitative polymerase chain reaction (qPCR). Furthermore, the identification of PI3K and PD-L1 in treated CRC cells were detected by western blotting analysis. PD-L1 presentation in HCT116 xenograft tumors was characterized by specialized immunohistochemistry (IHC) and the hematoxylin and eosin stain (H&E stain). The correlations between the change in PD-L1 expression and tumorigenic characteristics were also analyzed. (3) The PD-L1 was highly expressed in Colo_160224 rather than in the other three primary CRC cells and HCT-116 cells. Moreover, the PD-L1 expression was decreased by gefitinib (1 µM and 10 µM) in two cells (Colo_150624 and 160426), but 10 µM gefitinib stimulated PD-L1 expression in gefitinib-resistant primary CRC Colo_160224 cells. Inactivated PI3K reduced PD-L1 expression and proliferation in CRC Colo_160224 cells. Gefitinib didn’t inhibit PD-L1 expression and PI3K activation in gefitinib-resistant Colo_160224 cells. However, NDAT inhibited PI3K activation as well as PD-L1 accumulation in gefitinib-resistant Colo_160224 cells. The combined treatment of NDAT and gefitinib inhibited pPI3K and PD-L1 expression and cell proliferation. Additionally, NDAT reduced PD-L1 accumulation and tumor growth in the HCT116 (K-RAS mutant) xenograft experiment. (4) Gefitinib might suppress PD-L1 expression but did not inhibit proliferation through PI3K in gefitinib-resistant primary CRC cells. However, NDAT not only down-regulated PD-L1 expression via blocking PI3K activation but also inhibited cell proliferation in gefitinib-resistant CRCs

NDAT Targets PI3K-Mediated PD-L1 Upregulation to Reduce Proliferation in Gefitinib-Resistant Colorectal Cancer

The property of drug-resistance may attenuate clinical therapy in cancer cells, such as chemoresistance to gefitinib in colon cancer cells. In previous studies, overexpression of PD-L1 causes proliferation and metastasis in cancer cells; therefore, the PD-L1 pathway allows tumor cells to exert an adaptive resistance mechanism in vivo. Nano-diamino-tetrac (NDAT) has been shown to enhance the anti-proliferative effect induced by first-line chemotherapy in various types of cancer, including colorectal cancer (CRC). In this work, we attempted to explore whether NDAT could enhance the anti-proliferative effect of gefitinib in CRC and clarified the mechanism of their interaction. The MTT assay was utilized to detect a reduction in cell proliferation in four primary culture tumor cells treated with gefitinib or NDAT. The gene expression of PD-L1 and other tumor growth-related molecules were quantified by quantitative polymerase chain reaction (qPCR). Furthermore, the identification of PI3K and PD-L1 in treated CRC cells were detected by western blotting analysis. PD-L1 presentation in HCT116 xenograft tumors was characterized by specialized immunohistochemistry (IHC) and the hematoxylin and eosin stain (H&E stain). The correlations between the change in PD-L1 expression and tumorigenic characteristics were also analyzed. (3) The PD-L1 was highly expressed in Colo_160224 rather than in the other three primary CRC cells and HCT-116 cells. Moreover, the PD-L1 expression was decreased by gefitinib (1 µM and 10 µM) in two cells (Colo_150624 and 160426), but 10 µM gefitinib stimulated PD-L1 expression in gefitinib-resistant primary CRC Colo_160224 cells. Inactivated PI3K reduced PD-L1 expression and proliferation in CRC Colo_160224 cells. Gefitinib didn't inhibit PD-L1 expression and PI3K activation in gefitinib-resistant Colo_160224 cells. However, NDAT inhibited PI3K activation as well as PD-L1 accumulation in gefitinib-resistant Colo_160224 cells. The combined treatment of NDAT and gefitinib inhibited pPI3K and PD-L1 expression and cell proliferation. Additionally, NDAT reduced PD-L1 accumulation and tumor growth in the HCT116 (K-RAS mutant) xenograft experiment. (4) Gefitinib might suppress PD-L1 expression but did not inhibit proliferation through PI3K in gefitinib-resistant primary CRC cells. However, NDAT not only down-regulated PD-L1 expression via blocking PI3K activation but also inhibited cell proliferation in gefitinib-resistant CRCs