Platostoma palustre (Pp) jelly is a traditional food. Pp has been used as folk medicine and is effective against heat-shock, hypertension and diabetes. Therefore, the aim of this study was to evaluate the ethanolic extracts of Pp’ genotoxicity. The ethanolic extracts of Pp by using 40% ethanol for extraction. Evaluation of genotoxicity of ethanolic extracts of Pp by micronucleus assay was performed in vivo. During the in vivo genotoxicity-evaluated experiment, the experimental animal’s clinical behavior, body weight (BW), food consumption, and the percentage of RET/RBCs (reticulocytes/red blood cells) and MN-RET/RETs (micronucleated reticulocytes/reticulocytes) after the treatments of Pp ethanolic extracts were evaluated. Both sexes Institute of Cancer Research (ICR) mice were given three daily treatments by intraperitoneal injection of 2 mg/kg of mitomycin C (genotoxicity induction) or by oral route of 200 μL of PBS (normal control group). Until 48 h after the last treatment, K2-EDTA-anticoagulated peripheral blood specimens were collected. These blood samples were processed for the microscopy-based analysis using Giemsa stain and the percentage of reticulocytes and micronucleated reticulocytes was determined. The results were shown that the experimental animal’s clinical behaviors were normal in all groups. The BW and food consumption were no significant difference between all groups. RET/RBCs (‰) in male or female ICR mice in the negative control group, the normal control group, the high dose of Pp ethanolic extract group, the middle dose of Pp ethanolic extract group, and the low dose of Pp ethanolic extract group were respectively 7.8 ± 0.8 / 8.6 ± 0.8, 23.2 ± 1.5 / 22.1 ± 1.3, 22.8 ± 1.6 / 22.1 ± 1.7, 23.2 ± 1.5 / 22.6 ± 1.0 and 22.2 ± 1.9 / 23.9 ± 1.9; MN-RET/RETs (‰) in male or female ICR mice in the negative control group, the normal control group, the high dose of Pp ethanolic extract group, the middle dose of Pp ethanolic extract group, and the low dose of Pp ethanolic extract group were 2.0 ± 0.0 / 2.0 ± 0.0, 43.2 ± 10.6 / 39.6 ± 10.9, 1.8 ± 0.4 / 1.6 ± 0.5, 1.6 ± 0.5 / 1.4 ± 0.5, and 1.8 ± 0.4 / 1.6 ± 0.5, respectively. Both RET/RBCs (‰) and MN-RET/RETs (‰) in male or female ICR mice in the negative control group were significantly difference than the other groups (p < 0.001). Taken all results together, Pp ethanolic extracts were without genotoxicity. Therefore, Pp ethanolic extracts were safety.
Platostoma palustre jelly is a traditional food. Platostoma palustre has been used as folk medicine and is effective against heat-shock, hypertension and diabetes. Therefore, the aim of this study was to determine the effects of ethanolic extracts and commercial herbal tea of Platostoma palustre in inhibiting colorectal cancer cell viability. The ethanolic extracts of Platostoma palustre by using 90% ethanol for extraction. In this study, 2-fold serial dilution of 100 mg/mL Platostoma palustre extracts were applied. On other hand, the same dilution fold was also performed for 100% commercial herbal tea with Platostoma palustre. Additionally, CT-26 and HT-29 colorectal cancer cell lines were also used in this study. After co-culturing for 24 hours, the cell viability of CT-26 and HT-29 colorectal cancer cell lines were performed by using 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. According to these data, the 1.56-100 mg/mL Platostoma palustre extracts possessed the significant inhibition effects of CT-26 colorectal cancer cell viability. The 3.13-100% commercial herbal tea with Platostoma palustre possessed the significant inhibition effects of CT-26 colorectal cancer cell viability. The 6.25-100 mg/mL Platostoma palustre extracts possessed the significant inhibition effects of HT-29 colorectal cancer cell viability. The 25-100% commercial herbal tea with Platostoma palustre possessed the significant inhibition effects of HT-29 colorectal cancer cell viability. However, the 0.39-3.13 mg/mL Platostoma palustre extracts possessed the significant promoting effects of HT-29 colorectal cancer cell viability. The 0.39-12.5% commercial herbal tea with Platostoma palustre also possessed the significant promoting effects of HT-29 colorectal cancer cell viability. Comparison of CT-26 and HT-29 cell lines was on the cell viability after Platostoma palustre ethanolic extracts and commercial herbal tea treatments, CT-26 cell line was better sensitive than HT-29 cell line on the inhibition of cell viability after treatment of Platostoma palustre ethanolic extracts and the commercial herbal tea. Taken these results together, Platostoma palustre ethanolic extracts and commercial herbal tea may have a potential for inhibiting the growth of colorectal cancer cells.
Inflammatory bowel diseases (IBD) are multifactorial chronic intestinal disorders. Currently, mesalamine etc. and therapeutic strategies were suggested for IBD therapy. However, the etiology of IBD remains unclear which is an ongoing challenge and side effects of therapeutic drugs must be also considered. Thus, the aim of this study was to establish an optimal mouse model of IBD for the drug and therapeutic strategy investigations. Herein, 12 mice with 2% dextran sulfate sodium (DSS)-induced colitis (the negative control group) were via oral administration. Twelve mice were administered with drinking water without 2% DSS (the normal control group) via the same method as DSS-induced mice. At the end of the experiment, the body weight (BW), the stool appearance/status, the macroscopic and microscopic colonic injuries, and myeloperoxidase (MPO) activity were monitored, measured, and scored. The results showed that BALB/c mice’ BW decreased on D6-D8 of 2% DSS induction and then BALB/c mice’ BW continuously increased until D13 of the experiment. The stool appearance/status was seen soft stool on D2 of 2% DSS induction. The soft stool was mainly occurred on D2-D6 of 2% DSS induction. In addition, the watery stool was occurred on D4 of 2% DSS induction and was continuous until the end of the experiment (D14). The macroscopic colonic injuries were showed that colon length of the negative group (2% DSS-induced group) was significantly shorter than that of the normal control group (p < 0.001). The colon weight of the negative group was significantly increase than that of the normal control group (p < 0.001). The colon weight / length ratio in the negative group was significantly higher than that of the normal control group (p < 0.001). According to the histopathologic scores (evaluation of the microscopic colonic injuries), the scores of area, ulceration, inflammation, and edema in the colon tissues of the negative group was significantly higher than that of the normal control group (p < 0.001). The total histopathologic scores in the negative group was significantly higher than that of the normal control group (p < 0.001). The myeloperoxidase (MPO) activity in the inflamed colon tissue of the negative group was significantly higher than that of the normal control group (p < 0.001). Taken all results together, a DSS-induced ulcerative disease mouse model was successfully established. We hope that this animal model may be a useful tool for the research of the better therapeutics for IBD.
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