The complete chloroplast genomes of three Alismataceae species, including the medicinally important Alisma orientale.

Alismataceae is one of the early diverged families of monocotyledonous plants. We report the complete chloroplast genomes of three Alisma species, including Alisma orientale (Sam.) Juzep. 1934, A. subcordatum Raf. 1908, and A. triviale Pursh 1813, of which A. orientale is a traditional Chinese medical plant used widely to treat diuretics, diabetes, hepatitis, and inflammation. We sequenced the complete chloroplast genomes with the Illumina Nova-Seq 6000 platform using herbarium collections. The chloroplast genomes of A. orientale, A. subcordatum and A. triviale are 159,861 bp, 160,180 bp, and 159,727 bp in length, respectively. The three chloroplast genomes each contain 113 genes, including four rRNAs, 30 tRNAs genes, and 79 protein-coding genes, and the average GC content is 36.0%. Based on the whole chloroplast genomes of 19 species of Alismataceae and the close allies, the medicinally important A. orientale was found to be closely related to another medicinal plant Alisma plantago-aquatica L. 1753 in the phylogenetic analysis. The genus Alisma was supported to be monophyletic.

The protective effect of Schisandra chinensis (Turcz.) Baill. polysaccharide on DSS-induced ulcerative colitis in mice via the modulation of gut microbiota and inhibition of NF-κB activation.

BACKGROUND: Schisandra chinensis (Turcz.) Baill, a fruit utilized in traditional Chinese medicine (TCM), has a long history of medical application. It has been used to treat diseases of the gastrointestinal tract. Schisandra chinensis (Turcz.) Baill polysaccharide (SACP) is an important biologically active ingredient that has been shown to have a variety of beneficial effects including immune regulation and anti-oxidative properties. Ulcerative colitis (UC) is a complicated gastrointestinal inflammatory disease. We explore the protective effect of SACP against UC. RESULTS: Schisandra chinensis (Turcz.) Baill polysaccharide significantly reduced the disease activity index (DAI) and levels of myeloperoxidase(MPO) and malondialdehyde (MDA) in colonic tissue. It also alleviated weight loss and histopathological damage of mice. The expression of MUC2 and occludin proteins was increased and the barrier function of the colonic mucosa was enhanced by SACP treatment. NF-κB pathway activation was also inhibited and the production of pro-inflammatory cytokines was decreased whereas anti-inflammatory cytokines were increased. 16SrDNA sequencing of fecal flora showed that SACP increased the abundance of Muribaculaceaeunclassified, LachnospiraceaeNK4A136group and reduced the abundance of Bacteroides and Erysipelatoclostridium. CONCLUSION: Schisandra chinensis (Turcz.) Baill polysaccharide can protect against Dextran Sulfate Sodium Salt (DSS)-induced ulcerative colitis in mice. © 2023 Society of Chemical Industry.

Potato Preload Mitigated Postprandial Glycemic Excursion in Healthy Subjects: An Acute Randomized Trial.

This study investigated the preload effect of the medium and high glycemic index (GI) potato, as well as the combination of partially hydrolyzed guar gum (HG) and potato, when ingested prior to a rice meal, on the iso-carbohydrate basis. In a randomized crossover trial, 17 healthy female subjects consumed (1) rice; (2) co-ingestion of highly cooked potato (HP), and rice (HP + R); (3) co-ingestion of minimally cooked potato (MP) and rice (MP + R); (4) preload HP prior to rice meal (PHP + R); (5) preload MP prior to rice meal (PMP + R); (6) co-ingestion of partially hydrolyzed guar gum (HG), HP and rice (HG + HP + R); (7) preload HG prior to co-ingestion of HP and rice (PHG + HP + R); (8) co-preload of HG and HP prior to rice (PHG + PHP + R); and (9) preload of HP prior to co-ingestion of HG and rice (PHP + HG + R). Postprandial glycemic response (GR) tests and subjective satiety tests were conducted for each test food. Cooked potato as a preload to a rice meal could significantly cut the acute postprandial glycemic excursion by around 1.0 mmol/L, irrespective of the GI of the preload. Co-preload of partial hydrolyzed guar gum and highly cooked potato (PHG + PHP + R) resulted in improved acute GR in terms of peak glucose value and glycemic excursion compared with either HG preload or HP preload. All the meals with preload showed comparable or improved self-reported satiety. Within an equicarbohydrate exchange framework, both high-GI and medium-GI potato preload decreased the postprandial glycemic excursion in young healthy female subjects. The combination of HG and HP as double preload resulted in better GR than both single HG or HP preload did.

REM sleep deprivation induces endothelial dysfunction and hypertension in middle-aged rats: Roles of the eNOS/NO/cGMP pathway and supplementation with L-arginine.

Sleep loss can induce or aggravate the development of cardiovascular and cerebrovascular diseases. However, the molecular mechanism underlying this phenomenon is poorly understood. The present study was designed to investigate the effects of REM sleep deprivation on blood pressure in rats and the underlying mechanisms of these effects. After Sprague-Dawley rats were subjected to REM sleep deprivation for 5 days, their blood pressures and endothelial function were measured. In addition, one group of rats was given continuous access to L-arginine supplementation (2% in distilled water) for the 5 days before and the 5 days of REM sleep deprivation to reverse sleep deprivation-induced pathological changes. The results showed that REM sleep deprivation decreased body weight, increased blood pressure, and impaired endothelial function of the aortas in middle-aged rats but not young rats. Moreover, nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) concentrations as well as endothelial NO synthase (eNOS) phosphorylation in the aorta were decreased by REM sleep deprivation. Supplementation with L-arginine could protect against REM sleep deprivation-induced hypertension, endothelial dysfunction, and damage to the eNOS/NO/cGMP signaling pathway. The results of the present study suggested that REM sleep deprivation caused endothelial dysfunction and hypertension in middle-aged rats via the eNOS/NO/cGMP pathway and that these pathological changes could be inhibited via L-arginine supplementation. The present study provides a new strategy to inhibit the signaling pathways involved in insomnia-induced or insomnia-enhanced cardiovascular diseases.