Anti-obesity effects exerted by Dioscorea opposita Thunb. polysaccharides in diet-induced obese mice.

Obesity is characterized by chronic inflammation, insulin resistance, and gut microbiota dysbiosis. Dioscorea opposita Thunb. is a traditional food and medicine homolog from China. In the present study, polysaccharides isolated from a water extract of Dioscorea opposita Thunb. (DOTPs) were prepared. We showed that DOTPs reduced body weight, accumulation of fat tissues, insulin resistance, and inflammation in high-fat diet (HFD)-fed mice. Further experiments showed that DOTPs could regulate the composition of the gut microbiota in HFD mice. DOTPs supplementation in HFD-fed mice resulted in the reduction of the Firmicutes-to-Bacteroidetes ratio. We further demonstrated that DOTPs supplementation enhanced bacterial levels of Akkermansia and reduced levels of Ruminiclostridium_9. A significant reduction of glycolysis metabolism related to obesity and gut microbiota dysbiosis was also observed upon administration of DOTPs. Our results suggest that DOTPs can produce significant anti-obesity effects, by inhibiting systematic inflammation and ameliorating gut microbiota dysbiosis in diet-induced obese mice.

Lupeol triggers oxidative stress, ferroptosis, apoptosis and restrains inflammation in nasopharyngeal carcinoma via AMPK/NF-κB pathway.

OBJECTIVE: Nasopharyngeal carcinoma is a malignant tumor with high incidence in Asia. This study investigated the anti-tumor capacities of lupeol in nasopharyngeal carcinoma. METHODS: CCK-8 assay was employed to select the suitable concentration and intervention time of lupeol in 5-8 F and CNE1 cells. The anti-cancer impacts of lupeol were evaluated by flow cytometry, ROS generation, western blotting, ELISA, iron assay, lipid peroxidation, mitochondrial membrane potential (MMP), TUNEL, and immunohistochemistry assays. Additionally, levels of AMPK/NF-κB pathway-related proteins were tested by western blotting. RESULTS: Cell viability was notably decreased after administration of lupeol ≧ 20 µM. 20 µM and 40 µM lupeol induced cell apoptosis, enhanced oxidative stress and restrained immune response in nasopharyngeal carcinoma cells to some extent, as evidenced by the elevation of apoptotic rate, Bax and cleaved caspase-3 expression, ROS production and malondialdehyde level, and reduction of levels of Bcl-2, MMP, superoxide dismutase, TNF-α, IL-6 and IL-1ß. Also, lupeol promoted the iron secretion and lipid peroxidation, the effects of which were reversed by ferroptosis inhibitor (Fer-1). The inhibitory impacts of lupeol at the doses of 20 µM and 40 µM on glutathione and GPX4 levels were observed. Importantly, lupeol significantly elevated AMPKα phosphorylation, and reduced the levels of p-IκBα and nuclear NF-κB p65. Rescue assay stated that siAMPK could neutralize the above impacts of lupeol. Moreover, lupeol suppressed tumorigenesis of xenografts in nude mice. CONCLUSION: Lupeol exerted the anti-cancer impacts by inducing oxidative stress, ferroptosis and apoptosis, and suppressing inflammation via the AMPK/NF-κB pathway in nasopharyngeal carcinoma.

Anti-tumor effect of HOTAIR-miR-613-SNAI2 axis through suppressing EMT and drug resistance in laryngeal squamous cell carcinoma.

Laryngeal squamous cell carcinoma (LSCC) is the main pathological type of laryngeal cancer, which attacks the head and neck. Our present study aims to investigate the effect of long non-coding RNA (LncRNA) HOX transcript antisense RNA (HOTAIR) on epithelial mesenchymal transition (EMT) and drug resistance in LSCC. Firstly, the level of HOTAIR was found to be overexpressed in LSCC tissues compared with normal healthy tissues. Then, increased EMT and drug resistance were suppressed by specific HOTAIR shRNA effectively in LSCC cell lines. Besides, miR-613 was predicted to be a target of HOTAIR through bioinformatics analysis. Meanwhile, we found that a down-regulated level of miR-613 could be increased by HOTAIR shRNA and suppressed by LncRNA HOTAIR transfection in LSCC cells. The targeting relationship between miR-613 and HOTAIR was further demonstrated by a luciferase report assay. What is more, the inhibiting effect of HOTAIR shRNA on EMT and drug resistance was obviously abolished by the miR-613 inhibitor. Moreover, SNAI2, a critical regulator of EMT, was predicted as a target of miR-613 through bioinformatics analysis and luciferase report assays. As expected, the level of SNAI2 could be suppressed by HOTAIR shRNA and increased by the miR-613 inhibitor. Additionally, we discovered that SANI2 shRNA had similar inhibiting effect on EMT and drug resistance with HOTAIR shRNA in LSCC cells. Finally, the in vivo experiment further demonstrated that HOTAIR shRNA restricted tumor growth, EMT and drug resistance. Additionally, HOTAIR shRNA transfection could also increase the level of miR-613 and decrease the level of SNAI2 in vivo. Taken together, our research for the first time revealed the effect of the HOTAIR-miR-613-SNAI2 axis on EMT and drug resistance in LSCC, providing new targets for LSCC diagnosis and treatment.

Efficacy of chitosan dressing on endoscopic sinus surgery: a systematic review and meta-analysis.

Chitosan dressing might be promising to promote the recovery following endoscopic sinus surgery (ESS). However, the results remain controversial. We conducted a systematic review and meta-analysis to explore the influence of chitosan dressing on ESS. PubMed, EMbase, Web of science, EBSCO, and Cochrane library databases were systematically searched. Randomized controlled trials (RCTs) assessing the effect of chitosan dressing on endoscopic sinus surgery were included. Two investigators independently searched articles, extracted data, and assessed the quality of included studies. The primary outcomes were synechia and hemostasis. Meta-analysis was performed using random-effect model. Four RCTs involving 268 patients were included in the meta-analysis. Overall following ESS, compared with control intervention, chitosan dressing significantly reduced synechia (RR = 0.25; 95% CI 0.13-0.49; P < 0.0001) and promoted hemostasis (RR = 1.70; 95% CI 1.37-2.11; P < 0.00001), but showed no impact on granulations (RR = 1.18; 95% CI 0.72-1.95; P = 0.52), mucosal edema (RR = 0.88; 95% CI 0.60-1.29; P = 0.51), crusting (RR = 0.85; 95% CI 0.48-1.53; P = 0.60), and infection (RR = 0.88; 95% CI 0.51-1.52; P = 0.64). Compared to control intervention, chitosan dressing could significantly decrease edema and improve hemostasis, but had no effect on granulations, mucosal edema, crusting and infection.