Cleft palate is the most common facial birth defect worldwide. It is caused by environmental factors or genetic mutations. Environmental factors such as pharmaceutical exposure in women are known to induce cleft palate. The aim of the present study was to investigate the protective effect of Sasa veitchii extract against medicine-induced inhibition of proliferation of human embryonic palatal mesenchymal cells. We demonstrated that all-trans-retinoic acid inhibited human embryonic palatal mesenchymal cell proliferation in a dose-dependent manner, whereas dexamethasone treatment had no effect on cell proliferation. Cotreatment with Sasa veitchii extract repressed all-trans-retinoic acid-induced toxicity in human embryonic palatal mesenchymal cells. We found that cotreatment with Sasa veitchii extract protected all-trans-retinoic acid-induced cyclin D1 downregulation in human embryonic palatal mesenchymal cells. Furthermore, Sasa veitchii extract suppressed all-trans-retinoic acid-induced miR-4680-3p expression. Additionally, the expression levels of the genes that function downstream of the target genes ( ERBB2 and JADE1 ) of miR-4680-3p in signaling pathways were enhanced by cotreatment with Sasa veitchii extract and all-trans-retinoic acid compared to all-trans-retinoic acid treatment. These results suggest that Sasa veitchii extract suppresses all-trans-retinoic acid-induced inhibition of cell proliferation via modulation of miR-4680-3p expression.

Sasa veitchii (S. veitchii) is a traditional herb derived from the bamboo genus, which is collectively called Kumazasa. Although Kumazasa extract is believed to have various effects on the skin, there is little scientific evidence for these effects. In this study, we aimed to obtain scientific evidence regarding the wound-healing and skin-moisturizing effects of Kumazasa extract. Kumazasa extract was applied to the skin of a mouse wound model for 14 days, and the wound area and dermal water content were measured. Mice treated with Kumazasa extract had smaller wound areas than control mice. The dermal water content in the Kumazasa extract-treated group was significantly higher than that in the control group. The mRNA and protein expression levels of cutaneous aquaporin-3 (AQP3), which is involved in wound healing and increases in dermal water content, were significantly increased by treatment with Kumazasa extract. Kumazasa extract-treated HaCaT cells exhibited significantly higher AQP3 expression and p38 mitogen-activated protein kinase (MAPK) phosphorylation than control cells. With continuous application, Kumazasa extract increases AQP3 expression and exerts wound-healing and moisturizing effects. The increase in AQP3 expression elicited by Kumazasa extract may be due to enhancement of transcription via activation of p38 MAPK signaling.

Sasa veitchii and other Sasa species are traditional medicinal herbs belonging to a group of Japanese bamboos collectively called Kumazasa, and these species possess the potential for a wide variety of uses. The present study aimed to elucidate the anticancer mechanisms exerted by S. veitchii extract (SE) against a human breast cancer cell line, MCF-7 cells. Freeze-dried Sunchlon® was used as the SE, and cell proliferation activity was measured using the [3H]-thymidine incorporation assay. Induction of apoptosis was assessed via Annexin V and caspase-3 fluorescent staining, the induction of necrosis was measured via propidium iodide staining, and cell cycle-related protein expression was determined using western blotting. The IC50 value of the SE was 7.7 μg/mL in MCF-7 cells. Although the primary active ingredient in Sunchlon® is sodium copper chlorophyllin (0.25%), the present results indicated that ingredients other than SCC exert anti-cancer activities (the IC50 value of SCC was 715 μg/mL), and late apoptosis or necrosis was induced in an SE dose-dependent manner. The expression levels of cyclin D1 and Cdk6 were decreased after SE treatment, and there was no change in the Cdk1/2 expression levels. Additionally, the expression of the necrosis-related cell death indicators RIP1 and RIP3 was increased in response to high-dose SE treatments, and this was indicative of cells preparing for programmed cell death. SE induces cell death in MCF-7 cells via the inhibition of cyclin D1 expression at low concentrations, and this extract induces programmed necrosis (necroptosis) by potentiating RIP1/RIP3 expression.

BACKGROUND: The current study aimed to investigate the hepatoprotective effects of Sasa veitchii extract (SE) on carbon tetrachloride (CCl4)-induced liver fibrosis in mice.
METHODS: Male C57BL/6J mice were intraperitoneally injected with CCl4 dissolved in olive oil (1 g/kg) twice per week for 8 weeks. SE (0.1 mL) was administered orally once per day throughout the study, and body weight was measured weekly. Seventy-two hours after the final CCl4 injection, mice were euthanized and plasma samples were collected. The liver and kidneys were collected and weighed.
RESULTS: CCl4 administration increased liver weight, decreased body weight, elevated plasma alanine aminotransferase, and aspartate aminotransferase and increased liver oxidative stress (malondialdehyde and glutathione). These increases were attenuated by SE treatment. Overexpression of tumor necrosis factor-α was also reversed following SE treatment. Furthermore, CCl4-induced increases in α-smooth muscle actin, a marker for hepatic fibrosis, were attenuated in mice treated with SE. Moreover, SE inhibited CCl4-induced nuclear translocation of hepatic nuclear factor kappa B (NF-κB) p65 and phosphorylation of mitogen-activated protein kinase (MAPK).
CONCLUSIONS: These results suggested that SE prevented CCl4-induced hepatic fibrosis by inhibiting the MAPK and NF-κB signaling pathways.

The aim of this study was to investigate the therapeutic effect of Sasa veitchii leaf extract (SE) on features of obesity induced by a high-fat diet (HFD), such as hyperglycemia, insulin resistance, and inflammatory response. Four-week-old male ddY mice were freely fed HFD or control normal diet for 12 weeks; half was given SE in addition twice per day in weeks 8-12. Glucose and insulin intolerance were estimated, and body weight measured, weekly throughout the study. Following the experiment, the mice were fasted for 16 h, euthanized, and plasma was collected. Liver and epididymal adipose tissue was collected and weighed. Treatment with SE significantly decreased body weight, adipose tissue weight, plasma glucose, insulin, leptin, and tumor necrosis factor α compared with HFD groups, and markedly reduced the impairment of glucose and insulin tolerance in obese mice. Furthermore, hepatic steatosis and hepatic insulin receptor substrate were improved by treatment with SE. Our findings demonstrate that SE may reduce obesity-induced glucose and insulin tolerance, not only by suppressing inflammatory responses but also by improving insulin signaling.

We report lectin microarray profile of the polysaccharide fraction derived from Sasa veitchii leaf that exhibits anti-influenza activity. This fraction showed higher reactivities with lectins known as binders to oligo-mannose, fucose, or galactose. Our findings along with previously reported monosaccharide components suggest that the polysaccharide can be cross-reactive with cell surface receptors involved in immune system, thereby exerting anti-influenza activity.

OBJECTIVE: The aim of this study was to investigate the therapeutic effects of a Sasa veitchii leaf extract (SE) on carbon tetrachloride (CCl4)-induced hepato- and nephrotoxicity.
METHODS: Seven-week-old male ddy mice were orally administered SE or saline for seven days. Twenty-four hours after the last SE or saline administration, the mice were intraperitoneally injected with 3 g/kg CCl4 or olive oil. The mice from each group were euthanized and bled for plasma analysis 24 h after the CCl4/olive oil injection.
RESULTS: We found that pretreatment with SE completely abolished the CCl4-induced mortality in the mice after 24 h. The mice pretreated with SE exhibited significantly decreased levels of functional markers, and reduced histological damage in both the liver and the kidney. Furthermore, we found that the SE pretreatment decreased lipid peroxidation and calcium levels in the liver. Although SE could not induce the free radical-scavenging metallothioneins, the plasma biological antioxidant power was significantly increased in the mice pretreated with SE.
CONCLUSIONS: Our findings demonstrate that prophylactic treatment with SE protects mice from CCl4-induced lethal toxicity by decreasing oxidative stress in the liver and kidney, presumably by increasing biological antioxidant power.