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Purpose: To investigate the anticancer effects of the extract mixture of Mori radicis cortex, Mori ramulus, Angelica tenuissima, and Inonotus obliquus extract (MRME), a new herbal preparation from Korea, on B16F10 cells. Methods: The MRME was extracted with water. Cell Counting Kit-8 (CCK-8) assays and 4',6-diamidino-2-phenylindole (DAPI) staining were used to investigate the effect of MRME on cell proliferation and apoptosis in vitro. The expression of p53, p-p53, and phosphorylated Akt (p-Akt) were analyzed by western blotting. Wound-healing assay was used to analyze cell migration. Results: Based on CCK-8 and DAPI staining results, MRME inhibited the growth of B16F10 cells and induced apoptosis in B16F10 cells in a time- and dose-dependent manner (p < 0.05). MRME increased the expression of p53 and p-p53 and decreased the expression of p-Akt in a dose-dependent manner. MRME treatment inhibited cell migration and invasion (p < 0.05). Conclusion: Mori Radicis Cortex Mixture Extract exerts anticancer effect by inducing the expression of p53 and p-p53 and decreasing the expression of p-Akt, which may benefit patients with malignant melanoma when used in combination with v-raf murine sarcoma viral oncogene homolog B1 (BRAF) inhibitors. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) is an inflammation-associated common cancer worldwide. Paejang-san and Mori Cortex Radicis have been traditionally used for treating intestinal inflammatory diseases in Korea and China. In the present study, we developed a new herbal formula as an alternative to CRC treatments, which is composed of two main components of Paejangsan (Patriniae Radix (Paejang in Korean) and Coix Seed (Yiyiin in Korean)), and Mori Cortex Radicis (Sangbekpi in Korean) based on the addition and subtraction theory in traditional medicine, hence the name PSY, and explored the potential therapeutic effects of the new formula PSY in human CRC cells by analyzing viability, cell cycle and apoptosis. We found that PSY ethanol extract (EtOH-Ex), but not water extract, significantly suppressed the viability of human CRC cells, and synergistically decreased the cell proliferation compared to each treatment of Patriniae Radix and Coix Seed extract (PY) or Mori Cortex Radicis extract (S), suggesting the combination of PY and S in a 10-to-3 ratio for the formula PSY. PSY EtOH-Ex in the combination ratio reduced cell viability but induced cell cycle arrest at the G2/M and sub-G1 phases as well as apoptosis in CRC cells. In addition, the experimental results of Western blotting, immunofluorescence staining and reporter assays showed that PSY also inhibited STAT3 by reducing its phosphorylation and nuclear localization, which resulted in lowering STAT3-mediated transcriptional activation. In addition, PSY regulated upstream signaling molecules of STAT3 by inactivating JAK2 and Src and increasing SHP1. Moreover, the chemical profiles of PSY from UPLC-ESI-QTOF MS/MS analysis revealed 38 phytochemicals, including seven organic acids, eight iridoids, two lignans, twelve prenylflavonoids, eight fatty acids, and one carbohydrate. Furthermore, 21 potentially bioactive compounds were highly enriched in the PSY EtOH-Ex compared to the water extract. Together, these results indicate that PSY suppresses the proliferation of CRC cells by inhibiting the STAT3 signaling pathway, suggesting PSY as a potential therapeutic agent for treating CRC and 21 EtOH-Ex-enriched phytochemicals as anti-cancer drug candidates which may act by inhibiting STAT3. [ABSTRACT FROM AUTHOR]

In this study, the underlying mechanisms of metabolic syndrome (MetS) and the risk of AD factors, and the effect of dietary Mori cortex radicis (MCR) were investigated in two in vivo models. In glucose-induced C. elegans, MCR attenuated metabolic disorder by inhibiting lipid and advanced glycation end products (AGEs) production, reducing oxidative stress, and preventing cognition and behavioral deficits. In high fat/liquid sugar-induced MetS mice, MCR intervention improved metabolic alterations and spatial memory. Furthermore, MCR in diet suppressed AGEs deposit and RAGE expression, improved the antioxidant system, and decreased pro-inflammatory cytokine levels in mouse hippocampus. This was accompanied by downregulation of the MAPK (p38, ERK, and JNK) pathway, which consequently protected against brain damage by suppressing BACE-1, APP, Tau, and Aβ. These findings may be valuable for those investigating crosstalk between MetS and neurodegenerative disease progression or the effect of MCR on the AGE-RAGE/MAPK pathway.

Colorectal cancer (CRC) is an inflammation-associated common cancer worldwide. Paejang-san and Mori Cortex Radicis have been traditionally used for treating intestinal inflammatory diseases in Korea and China. In the present study, we developed a new herbal formula as an alternative to CRC treatments, which is composed of two main components of Paejangsan (Patriniae Radix (Paejang in Korean) and Coix Seed (Yiyiin in Korean)), and Mori Cortex Radicis (Sangbekpi in Korean) based on the addition and subtraction theory in traditional medicine, hence the name PSY, and explored the potential therapeutic effects of the new formula PSY in human CRC cells by analyzing viability, cell cycle and apoptosis. We found that PSY ethanol extract (EtOH-Ex), but not water extract, significantly suppressed the viability of human CRC cells, and synergistically decreased the cell proliferation compared to each treatment of Patriniae Radix and Coix Seed extract (PY) or Mori Cortex Radicis extract (S), suggesting the combination of PY and S in a 10-to-3 ratio for the formula PSY. PSY EtOH-Ex in the combination ratio reduced cell viability but induced cell cycle arrest at the G2/M and sub-G1 phases as well as apoptosis in CRC cells. In addition, the experimental results of Western blotting, immunofluorescence staining and reporter assays showed that PSY also inhibited STAT3 by reducing its phosphorylation and nuclear localization, which resulted in lowering STAT3-mediated transcriptional activation. In addition, PSY regulated upstream signaling molecules of STAT3 by inactivating JAK2 and Src and increasing SHP1. Moreover, the chemical profiles of PSY from UPLC-ESI-QTOF MS/MS analysis revealed 38 phytochemicals, including seven organic acids, eight iridoids, two lignans, twelve prenylflavonoids, eight fatty acids, and one carbohydrate. Furthermore, 21 potentially bioactive compounds were highly enriched in the PSY EtOH-Ex compared to the water extract. Together, these results indicate that PSY suppresses the proliferation of CRC cells by inhibiting the STAT3 signaling pathway, suggesting PSY as a potential therapeutic agent for treating CRC and 21 EtOH-Ex-enriched phytochemicals as anti-cancer drug candidates which may act by inhibiting STAT3.

Norovirus is a major cause of acute gastroenteritis globally, resulting in enormous health and societal costs. In this study, the antiviral activities of Mori Cortex Radicis (MCR) extract and its bioactive flavonoids, morusin and kuwanon G, were tested against murine norovirus (MNV), a human norovirus surrogate, using plaque assay. The antiviral activity was confirmed in simulated digestive conditions, including simulated saliva fluid (SSF), simulated gastric fluid (SGF), and simulated intestinal fluid (SIF). Pre-treatment of MNV with MCR extract at 1000 µg/mL showed antiviral activity with a 1.1-log reduction. Morusin and kuwanon G also demonstrated a 1.0-log and 0.6-log reductions of MNV titers, respectively, at 100 µM. MCR extract at a concentration of 2 mg/mL in SSF, SGF, and SIF markedly reduced MNV titers by 1.8, 1.9, and 1.5 logs, respectively. Therefore, these data suggest that MCR extract can be used to control norovirus infectivity. [ABSTRACT FROM AUTHOR]

Present study was conducted to investigate ameliorating effects of Mori Cortex radicis on cognitive impair and neuronal defects in HFD-induced (High Fat Diet-Induced) obese mice. To induce obesity, C57BL/6 mice were fed an HFD for 8 weeks, and then mice were fed the HFD plus Mori Cortex radicis extract (MCR) (100 or 200 mg/kg/day) for 6 weeks. Prior to sacrifice, body weights were measured, and Y-maze test and oral glucose tolerance test were performed. Serum lipid metabolic biomarkers (TG, LDL, and HDL/total cholesterol ratio) and antioxidant enzymes (glutathione, superoxide dismutase, and catalase), malondialdehyde (MDA), and acetylcholinesterase (AChE) levels were measured in brain tissues. The expressions of proteins related to insulin signaling (p-IRS, PI3K, p-Akt, and GLUT4) and neuronal protection (p-Tau, Bcl-2, and Bax) were examined. MCR suppressed weight gain, improved serum lipid metabolic biomarker and glucose tolerance, inhibited AChE levels and MDA production, and restored antioxidant enzyme levels in brain tissue. In addition, MCR induced neuronal protective effects by inhibiting p-Tau expression and increasing Bcl-2/Bax ratio, which was attributed to insulin-induced increases in the expressions p-IRS, PI3K, p-Akt, and GLUT4. These indicate MCR may reduce HFD-induced insulin dysfunction and neuronal damage and suggest MCR be considered a functional material for the prevention of T2DM-associated neuronal disease.

[Display omitted] • MCR suppressed lipid and AGEs accumulation and ROS, and improved cognitive functions in glucose-fed C. elegans. • MCR attenuated metabolic disorder and spatial memory in high fat/liquid sugar diet-fed mouse. • Diet-induced MetS mouse model increased AGEs deposit, pro-inflammatory cytokines and AD-related factors. • These MetS derived neuronal damages was inhibited by MCR intake via AGE-RAGE/MAPK pathway. In this study, the underlying mechanisms of metabolic syndrome (MetS) and the risk of AD factors, and the effect of dietary Mori cortex radicis (MCR) were investigated in two in vivo models. In glucose-induced C. elegans , MCR attenuated metabolic disorder by inhibiting lipid and advanced glycation end products (AGEs) production, reducing oxidative stress, and preventing cognition and behavioral deficits. In high fat/liquid sugar-induced MetS mice, MCR intervention improved metabolic alterations and spatial memory. Furthermore, MCR in diet suppressed AGEs deposit and RAGE expression, improved the antioxidant system, and decreased pro-inflammatory cytokine levels in mouse hippocampus. This was accompanied by downregulation of the MAPK (p38, ERK, and JNK) pathway, which consequently protected against brain damage by suppressing BACE-1, APP, Tau, and Aβ. These findings may be valuable for those investigating crosstalk between MetS and neurodegenerative disease progression or the effect of MCR on the AGE-RAGE/MAPK pathway. [ABSTRACT FROM AUTHOR]

Present study was conducted to investigate ameliorating effects of Mori Cortex radicis on cognitive impair and neuronal defects in HFD-induced (High Fat Diet-Induced) obese mice. To induce obesity, C57BL/6 mice were fed an HFD for 8 weeks, and then mice were fed the HFD plus Mori Cortex radicis extract (MCR) (100 or 200 mg/kg/day) for 6 weeks. Prior to sacrifice, body weights were measured, and Y-maze test and oral glucose tolerance test were performed. Serum lipid metabolic biomarkers (TG, LDL, and HDL/total cholesterol ratio) and antioxidant enzymes (glutathione, superoxide dismutase, and catalase), malondialdehyde (MDA), and acetylcholinesterase (AChE) levels were measured in brain tissues. The expressions of proteins related to insulin signaling (p-IRS, PI3K, p-Akt, and GLUT4) and neuronal protection (p-Tau, Bcl-2, and Bax) were examined. MCR suppressed weight gain, improved serum lipid metabolic biomarker and glucose tolerance, inhibited AChE levels and MDA production, and restored antioxidant enzyme levels in brain tissue. In addition, MCR induced neuronal protective effects by inhibiting p-Tau expression and increasing Bcl-2/Bax ratio, which was attributed to insulin-induced increases in the expressions p-IRS, PI3K, p-Akt, and GLUT4. These indicate MCR may reduce HFD-induced insulin dysfunction and neuronal damage and suggest MCR be considered a functional material for the prevention of T2DM-associated neuronal disease. [ABSTRACT FROM AUTHOR]