Promising research has explored yoga as a sound option to help address the stress-related psychological symptoms that come with tinnitus

PMID: 

Molecules. 2019 Dec 17 ;24(24). Epub 2019 Dec 17. PMID: 31861064

Abstract Title: 

Polyphenol Extracts from Three Colombian Passifloras (Passion Fruits) Prevent Inflammation-Induced Barrier Dysfunction of Caco-2 Cells.

Abstract: 

Chronic intestinal inflammation is associated with pathophysiology of obesity and inflammatory bowel diseases. Gastrointestinal inflammation increases barrier dysfunction exacerbating the immune response and perpetuating chronic inflammation. Anti-inflammatory flavonoids may prevent this intestinal barrier dysfunction. The purpose of this study was to evaluate the polyphenol composition of Colombianvar. Flavicarpa (Maracuyá),var. Sims (Gulupa), andvar. Juss (Granadilla) (passion fruits) and to evaluate their ability to inhibit disruption of intestinal barrier dysfunction of Caco-2 (colorectal adenocarcinoma) cells by an inflammatory cocktail (IC). Polyphenols (flavan-3-ols, phenolic acids, flavonols), xanthenes, and a terpene were identified in passion fruits. Cyanidin 3-rutinoside, (+)-catechin and ferulic acid were the most abundant phenolics in.var. Flavicarpa,var. Sims, andvar. Juss, respectively. Fruit extracts prevented loss of transepithelial electrical resistance in Caco-2 cells treated with the IC. Among the extracts,var. Juss was most effective at maintaining Caco-2 transepithelial electrical resistance (TEER) with ~73% relative to the IC-treated cells with about 43% of initial TEER values. This fruit had cyanidin-3-rutinoside, (+)-catechin, (-)-epicatechin, and ferulic acid in its phenolic profile. Results of this work support the hypothesis that consumption of passion fruit extracts could benefit intestinal health.

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PMID: 

Antibiotics (Basel). 2019 Dec 23 ;9(1). Epub 2019 Dec 23. PMID: 31877915

Abstract Title: 

The Structure Features and Improving Effects of Polysaccharide fromon Antibiotic-Associated Diarrhea.

Abstract: 

() is often used as a medical and food resource in China. The present study was designed to investigate the features and effects of polysaccharide from(WAP) on rats with antibiotic-associated diarrhea (AAD). WAP was mainly composed of glucose, galactose, arabinose and glacturonic acid, with glucan, arabinogalactan and RG-I regions, and it showed loosely irregular sheet conformation. WAP decreased the inflammatory cell infiltration of colon in AAD rats, increased propionate and butyrate production, improved metabolic levels, adjusted the diversity and composition of gut microbiota, increased the relative abundance of, and decreased the relative abundance ofand. In conclusion, WAP contained different types of polysaccharide regions and sheet three-dimensional conformation, while it ameliorated AAD by recovering the colon structure, adjusting the gut microbiota, and improving the SCFAs levels. The results can provide some data basis for natural products to alleviate the side effects related to antibiotics.

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PMID: 

BMC Complement Altern Med. 2019 Dec 5 ;19(1):355. Epub 2019 Dec 5. PMID: 31805910

Abstract Title: 

Astragaloside IV protects against diabetic nephropathy via activating eNOS in streptozotocin diabetes-induced rats.

Abstract: 

BACKGROUND: Astragaloside IV (AS-IV) was reported to play a role in improving diabetic nephropathy (DN), however, the underlying mechanisms still remain unclear. The aim of the present study is to investigate whether AS-IV ameliorates DN via the regulation of endothelial nitric oxide synthase (eNOS).METHODS: DN model was induced in Sprague-Dawley (SD) male rats by intraperitoneal injection of 65 mg/kg streptozotocin (STZ). Rats in the AS-IV treatment group were orally gavaged with 5 mg/kg/day or 10 mg/kg/day AS-IV for eight consecutive weeks. Body weight, blood glucose, blood urea nitrogen (BUN), Serum creatinine (Scr), proteinuria and Glycosylated hemoglobin (HbA1c) levels were measured. Hematoxylin-Eosin (HE) and Periodic Acid-Schiff (PAS) staining were used to detect the renal pathology. The apoptosis status of glomerular cells was measured by TUNEL assay. The phosphorylation and acetylation of eNOS were detected by western blot. The effects of AS-IV on high-glucose (HG)-induced apoptosis and eNOS activity were also investigated in human renal glomerular endothelial cells (HRGECs) in vitro.RESULTS: Treatment with AS-IV apparently reduced DN symptoms in diabetic rats, as evidenced by reduced BUN, Scr, proteinuria, HbA1c levels and expanding mesangial matrix. AS-IV treatment also promoted the synthesis of nitric oxide (NO) in serum and renal tissues and ameliorated the phosphorylation of eNOS at Ser 1177 with decreased eNOS acetylation. Moreover, HG-induced dysfunction of HRGECs including increased cell permeability and apoptosis, impaired eNOS phosphorylation at Ser 1177, and decreased NO production, were all reversed by AS-IV treatment.CONCLUSIONS: These novel findings suggest that AS-IV ameliorates functional abnormalities of DN through inhibiting acetylation of eNOS and activating its phosphorylation at Ser 1177. AS-IV could be served as a potential therapeutic drug for DN.

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PMID: 

Int J Mol Sci. 2019 Dec 5 ;20(24). Epub 2019 Dec 5. PMID: 31817362

Abstract Title: 

Astragaloside IV Protects Against Oxidative Stress in Calf Small Intestine Epithelial Cells via NFE2L2-Antioxidant Response Element Signaling.

Abstract: 

Oxidative stress can damage intestinal epithelial cell integrity and function, causing gastrointestinal disorders. Astragaloside IV (ASIV) exhibits a variety of biological and pharmacological properties, including anti-inflammatory and antioxidant effects. The purpose of this research was to investigate the cytoprotective action of ASIV and its mechanisms in calf small intestine epithelial cells with hydrogen peroxide (HO)-induced oxidative stress. ASIV pretreatment not only increased cell survival, but it also decreased reactive oxygen species generation and apoptosis, enhanced superoxide dismutase, catalase, and glutathione peroxidase levels, and it reduced malondialdehyde formation. Furthermore, pretreatment with ASIV elevated the mRNA and protein levels of nuclear factor erythroid 2-related factor 2 (NFE2L2), heme oxygenase-1 (HMOX1), and NAD(P)H quinone dehydrogenase 1 (NQO1). The NFE2L2 inhibitor ML385 inhibited NFE2L2 expression and then blocked HMOX1 and NQO1 expression. These results demonstrate that ASIV treatment effectively protects against HO-induced oxidative damage in calf small intestine epithelial cells through the activation of the NFE2L2-antioxidant response element signaling pathway.

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PMID: 

Phytother Res. 2019 Dec 10. Epub 2019 Dec 10. PMID: 31823428

Abstract Title: 

Astragaloside IV reverses simvastatin-induced skeletal muscle injury by activating the AMPK-PGC-1α signalling pathway.

Abstract: 

In this study, we investigated the effect of astragaloside IV on skeletal muscle energy metabolism disorder caused by statins and explored the possible mechanisms. High-fat diet-fed apolipoprotein E knockout (ApoE) mice performed aerobic exercise and were administered simvastatin, simvastatin + trimetazidine, or simvastatin + astragaloside IV by gavage. At the end of treatment, exercise performance was assessed by the hanging grid test, forelimb grip test, and running tolerance test. Moreover, plasma lipid and creatine kinase concentrations were measured. After sacrifice, the gastrocnemius muscle was used to assess muscle morphology, and energy metabolism was evaluated by determining the concentration of lactic acid and the storage capacity of adenosine triphosphate and glycogen. Mitochondrial function was assessed by measuring mitochondrial complex III and citrate synthase activity and membrane potential. In addition, oxidative stress was assessed by determining the level of hydrogen peroxide. Finally, using western blotting and reverse transcription polymerase chain reaction, we explored the mechanism of astragaloside IV in alleviating simvastatin-induced muscle injury. Our results demonstrated that astragaloside IV reversed simvastatin-induced muscle injury without affecting the lipid-lowering effect of simvastatin. Moreover, astragaloside IV promoted the phosphorylation of AMPK and activated PGC-1α, which upregulated the expression of NRF1 to enhance energy metabolism and inhibit skeletal muscle cell apoptosis.

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PMID: 

Pharmacology. 2019 Dec 11:1-9. Epub 2019 Dec 11. PMID: 31825924

Abstract Title: 

Astragaloside IV Alleviates Cerebral Ischemia-Reperfusion Injury by Activating the Janus Kinase 2 and Signal Transducer and Activator of Transcription 3 Signaling Pathway.

Abstract: 

Astragaloside IV (AS-IV) is an active component extracted from the traditional Chinese herbal medicine. AS-IV is a neuroprotective component in cerebral ischemic models. However, roles of AS-IV in cerebral ischemia-reperfusion (I/R) injury and the underlying mechanisms are rarely investigated. The role of AS-IV in oxygen – glucose deprivation reoxygenation (OGD/R)-induced cell proliferation and apoptosis assays were analyzed by Cell Counting Kit-8 and Flow cytometric. Western Blot assays were performed to measure the related expression levels in SH-SY5Y cells. Meanwhile, activities of reactive oxygen species (ROS), superoxide dismutase (SOD), and malondialdehyde (MDA) in OGD/R-induced cells were determined by relative commercial kits. AS-IV was also used in cerebral I/R rat model, aimed to investigate the effects on cerebral infarct. The results indicated that OGD/R suppressed viability, enhanced apoptosis, which could be reversed by AS-IV treatment. Compared with the control group, the expression of p-JAK2 and p-STAT3 was significantly increased by AS-IV (60μg/mL) under the OGD/R condition. Furthermore, AS-IV (60 μg/mL) treatment markedly increased SOD activity, whereas significantly decreased MDA activity and production of ROS in OGD/R-induced cells. The protective effects of AS-IV mentioned above were weaken or abolished while adding JAK2 inhibitorAG490. In addition, the effects of AS-IV on Janus kinase 2 and signal transducer and activator of transcription 3 (JAK2/STAT3) signaling in cerebral I/R injury were also verified in vivo. AS-IV protected against cerebral I/R injury and reversed by AG490. Therefore, in vitro and in vivo analyses suggested that AS-IV may protect against cerebral I/R injury partly mediated by JAK2/STAT3 signaling pathway and antioxidative effects. AS-IV may serve as a novel therapeutic regimen for cerebral I/R injury.

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PMID: 

Front Pharmacol. 2019 ;10:1388. Epub 2019 Nov 28. PMID: 31849654

Abstract Title: 

Astragaloside IV Exerts Cardioprotection in Animal Models of Viral Myocarditis: A Preclinical Systematic Review and Meta-Analysis.

Abstract: 

Astragaloside IV (AS-IV), the essential active component of astragalus, possesses diverse biological activities that have beneficial effects against cardiovascular disease. Here, we conducted a preclinical systematic review of 15 studies including 577 animals to establish the efficacy and potential mechanisms of AS-IV for animal models of viral myocarditis (VM). Six databases were searched from inception to October 2018. Application of the Cochrane Collaboration's tool 10-item checklist and Rev-Man 5.3 software to analyze risk of bias of studies and data on outcome measures revealed study quality scores ranging from 2 to 5. Compared with the control group, AS-IV induced a marked decrease in mortality (P

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PMID: 

Int Immunopharmacol. 2019 Dec 9 ;78:106066. Epub 2019 Dec 9. PMID: 31835087

Abstract Title: 

Astragaloside IV attenuates sepsis-induced intestinal barrier dysfunction via suppressing RhoA/NLRP3 inflammasome signaling.

Abstract: 

Intestinal barrier dysfunction is a trigger for sepsis progression. NLRP3 inflammasome and RhoA contribute to sepsis and intestinal inflammation. The current study aimed to explore the effects of Astragaloside IV (AS-IV), a bioactive compound from Astragalus membranaceus, on sepsis-caused intestinal barrier dysfunction and whether NLRP3 inflammasome and RhoA are involved. Septic mice modeled by cecal ligation and puncture (CLP) operation were administered with 3 mg/kg AS-IV intravenously. AS-IV decreased mortality, cytokines release, I-FABP secretion, intestinal histological score and barrier permeability, and increased tight junction (TJ) expression in intestine in CLP model. Also, in Caco-2 cells subjected to lipopolysaccharide (LPS), 200 μg/mL AS-IVco-incubation reduced cytokines levels and enhanced in vitro gut barrier function without cytotoxicity. Subsequently, NLRP3 inflammasome and RhoA were highly activated both in intestinal tissue in vivo and in Caco-2 cells in vitro, both of which were significantly suppressed by AS-IV treatment. In addition, the benefits of AS-IV on Caco-2 monolayer barrier were largely counteracted by RhoA agonist CN03 and NLRP3 gene overexpression, respectively. Furthermore, LPS-induced NLRP3 inflammasome activation was abrogated by RhoA inhibitor C3 exoenzyme. However, NLRP3 knockdown by siRNA hardly affected RhoA activation in Caco-2 cells. These data suggest that AS-IV protects intestinal epithelium from sepsis-induced barrier dysfunction via inhibiting RhoA/NLRP3 inflammasome signal pathway.

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PMID: 

Eur J Pharmacol. 2019 Jul 5 ;854:289-297. Epub 2019 Apr 17. PMID: 31004602

Abstract Title: 

Tetramethylpyrazine attenuates blood-brain barrier disruption in ischemia/reperfusion injury through the JAK/STAT signaling pathway.

Abstract: 

Tetramethylpyrazine (TMP) has been studied in depth and is widely used in the treatment of many kinds of diseases in China. However, whether it has neuroprotective effects on cerebral ischemia remains unclear. An ischemia/reperfusion (I/R) injury animal model was established via middle cerebral artery occlusion in this study. We set several different groups in which the rats were performed in different ways to explore the effects of TMP on blood-brainbarrier (BBB) disruption and determine whether TMP relieved BBB disruption through blocking the JAK/STAT signaling pathway. Our results showed that TMP could reduce the neurological functional loss, decrease the brain edema and BBB permeability, as well as increase the expression of tight junction proteins via inhibiting the activation of JAK/STAT signaling pathway. Overall, we demonstrated that TMP promoted neurological recovery after I/R injury via restoring the integrity and function of BBB.

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