Astragaloside IV protects against the pathological cardiac hypertrophy in mice.

Although pathologic hypertrophic hearts currently maintain output, sustained cardiac hypertrophy could predispose a patient to arrhythmia and sudden death, and also cause heart failure. Thus, finding effective treatment and exploring the underlying molecular mechanisms of cardiac hypertrophy is urgently necessary. Astragaloside IV (AST-IV) is the main active component, extracted from the traditional Chinese medicinal herb Astragalus membranaceus. Previous studies have indicated that AST-IV has various bioactivities, such as anti-cancer, anti-oxidative stress and anti-inflammation. In the present study, we aimed to explore the effects of AST-IV on cardiac hypertrophy induced by aortic banding (AB) surgery in mice, and to reveal the underlying signaling mechanisms. The suppressor of IKKε (SIKE) is a negative regulator of the interferon pathway, which could be enhanced by AST-IV to ameliorate pathological cardiac hypertrophy in mice through inactivating TANK-binding kinase 1 (TBK1)/PI3K/AKT signaling pathway. AST-IV attenuated cardiac hypertrophy, collagen accumulation and abnormal cardiac functions. In addition, AB-induced apoptosis and inflammation in the heart tissue samples of mice, which were attenuated by AST-IV administration through inhibiting SIKE expression levels. Together, the findings above indicated that AST-IV might be a potential candidate to prevent cardiac hypertrophy via elevating SIKE to suppress TBK1/PI3K/AKT activity.

Therapeutic effects of Lactobacillus casei Qian treatment in activated carbon-induced constipated mice.

In the present study, the therapeutic effects of Lactobacillus casei Qian (LC-Qian), the key microorganism in Tibetan yak yoghurt, on activated carbon-induced constipation were determined in vivo. ICR mice were treated with LC-Qian for nine days by oral administration. The body weight, defecation status, gastrointestinal transit and defecation time of mice were assessed, and the serum levels of motilin (MTL), gastrin (Gas), endothelin (ET), somatostatin (SS), acetylcholinesterase (AChE), substance P (SP) and vasoactive intestinal peptide (VIP) were further evaluated. Bisacodyl was used as the positive control. The time until the first black stool defecation following carbon intake of the normal, control, 100 mg/kg bisacodyl-treated, Lactobacillus bulgaricus (LB)-treated, LC-Qian (L)-and LC-Qian (H)-treated mice was 93, 231, 121, 194, 172 and 157 min, respectively. Following treatment with LC-Qian, the gastrointestinal transit was increased to 52.4% [LC-Qian (L)] and 65.8% [LC-Qian (H)], while that in the group treated with the common lactic acid bacteria of LB was 40.3%. The MTL, Gas, ET, AChE, SP and VIP serum levels were significantly increased and levels of SS were reduced in mice following LC-Qian treatment compared with those in the control mice (P<0.05). Reverse transcription quantitative polymerase chain reaction indicated that LC-Qian raised the c-Kit, GDNF as well as SCF mRNA expression levels and reduced the TRPV1 and NOS expression levels in tissue of the small intestine in mice. These results suggested that lactic acid bacteria prevent constipation in mice, among which LC-Qian was the most effective.