Mao Jian Tea (MJT) has been generally consumed as a digestive aid for more than a hundred years in the Shanxi province of China. However, determination of its efficacy still remains elusive. This study investigated the effect of Mao Jian Green Tea (MJGT) on gastrointestinal motility. The biphasic effects of the hydro extracts of MJGT on gastric emptying and small intestinal propulsion of rats were identified in vivo; namely, the low (MJGT_L) and medium (MJGT_M) concentrations promoted gastrointestinal motility (p < 0.05), whereas the high concentration (MJGT_H) showed the opposite effect (p < 0.01). The expression levels of the gastric hormones, GAS, MTL and VIP (p < 0.05) were consistent with the gastrointestinal motility variation, with the exception of MTL in MJGT_H group (p > 0.01). Two flavonoids, eriodictyol (0.152 mg/mL) and luteolin (0.034 mg/mL), and the corresponding glycosides eriodictyol-7-O-glucoside (0.637 mg/mL) and luteolin-7-O-glucoside (0.216 mg/mL), dominated the hydro extracts identified by HPLC and UPLC-ESI-MS. These compounds can regulate the muscle strip contractions isolated from the gastrointestinal tissues. Additionally, the different concentrations also influenced the gut microbiota accordingly characterized by 16S rDNA gene sequencing. The MJGT_L boosted several probiotic bacteria, such as Muribaculaceae (1.77-fold), Prevotellaceae (1.85-fold) and Lactobacillaceae (2.47-fold), and suppressed the pathogenic species such as Staphylococcaceae (0.03-fold) that, conversely, was enriched in the MJGT_H group (1.92-fold). Therefore, the biphasic effect indicated that the dosage of the herbal tea should not be overlooked.

BACKGROUND: To understand the relationship between myocardial contractility and external stimuli, detecting ex vivo myocardial contractility is necessary.
METHODS: We elaborated a method for contractility detection of isolated C57 mouse papillary muscle using Myostation-Intact system under different frequencies, voltages, and calcium concentrations.
RESULTS: The results indicated that the basal contractility of the papillary muscle was 0.27 ± 0.03 mN at 10 V, 500-ms pulse duration, and 1 Hz. From 0.1 to 1.0 Hz, contractility decreased with an increase in frequency (0.45 ± 0.11-0.10 ± 0.02 mN). The voltage-initiated muscle contractility varied from 3 to 6 V, and the contractility gradually increased as the voltage increased from 6 to 10 V (0.14 ± 0.02-0.28 ± 0.03 mN). Moreover, the muscle contractility increased when the calcium concentration was increased from 1.5 to 3 mM (0.45 ± 0.17-1.11 ± 0.05 mN); however, the contractility stopped increasing even when the concentration was increased to 7.5 mM (1.02 ± 0.23 mN).
CONCLUSIONS: Our method guaranteed the survivability of papillary muscle ex vivo and provided instructions for Myostation-Intact users for isolated muscle contractility investigations.

Polycystic ovary syndrome (PCOS), a common hormonal disorder in women, affects 4-18% of women of reproductive age worldwide. A higher prevalence of irritable bowel syndrome was found in women with PCOS. However, the effects and mechanism of PCOS on stomach and colon contractility remain unclear.
This study aims to evaluate the correlation between PCOS and gastrointestinal disorder.
Four-week-old female rats were subcutaneously implanted with pellets containing 7.5 mg of dihydrotestosterone for 13 weeks to create PCOS rat models. After vaginal smears, the estrus cycle stage was evaluated. Oral glucose tolerance test was performed after 90 days of treatment. All animals were killed at 17 weeks. The rats were fasted overnight and then anesthetized before decapitation, and the stomach fundus and colon were surgically removed and cultured in oxygenated Krebs solution. Acetylcholine and carbachol were used to evaluate the cholinergic system on contractility.
The basal and stomach fundus responded with a reduced frequency and contractility in response to acetylcholine in the PCOS group. Moreover, no difference was found in the spontaneous stomach contractility induced by carbachol in both groups. Lower maximal colon muscle contractility was also found in response to acetylcholine stimulation in PCOS rats. Furthermore, lower maximal muscle contractility was found in response to extracellular calcium levels. MLC20 phosphorylation was also reduced in the gastrointestinal tissue in PCOS rats.
PCOS induces gastroparesis and reduces gastrointestinal muscle contractility. This effect is, at least partly, through reducing the responsiveness of acetylcholine and MLC20 phosphorylation.

KCNQ1 encodes a potassium voltage-gated channel and represents a susceptibility locus for type 2 diabetes mellitus (T2DM). Here, we explored the association between KCNQ1 polymorphisms and hypertension risk in individuals with T2DM, as well as the role of KCNQ1 in vascular smooth muscle cell contraction in vitro. To investigate the relationship between KCNQ1 and the risk of developing hypertension in patients with T2DM, we divided the T2DM cohort into hypertension (n = 452) and non-hypertension (n = 541) groups. The Mann-Whitney U test, chi-square test, and multivariate regression analyses were used to assess the clinical characteristics and genotypic frequencies. In vitro studies utilized the rat aortic smooth muscle A10 cell line. Patients in the hypertension group were significantly older at the time of enrollment and had higher levels of body mass index, waist-to-hip ratio, and triglyceride than those in the non-hypertension group. The KCNQ1 rs3864884 and rs12576239 genetic variants were associated with hypertension in T2DM. KCNQ1 expression was lower in the individuals with the CC versus the CT and TT genotypes. Smooth muscle cell contractility was inhibited by treatment with a KCNQ1 inhibitor. These results suggest that KCNQ1 might be associated with hypertension in individuals with T2DM.