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Your search keyword '"Luo, Xiu-Ju"' showing total 4 results
Start Over Author "Luo, Xiu-Ju" Journal planta medica
4 results on '"Luo, Xiu-Ju"'

1. Magnesium Lithospermate B Derived from Salvia miltiorrhiza Ameliorates Right Ventricle Remodeling in Pulmonary Hypertensive Rats via Inhibition of NOX/VPO1 Pathway.

Author

Li, Tao, Peng, Jing-Jie, Wang, E-Li, Li, Nian-Sheng, Song, Feng-Lin, Yang, Jin-Fu, Luo, Xiu-Ju, Liu, Bin, and Peng, Jun

Subjects
ANIMAL experimentation, ANTI-inflammatory agents, ANTIOXIDANTS, CELLULAR signal transduction, GENE expression, RIGHT heart ventricle, HERBAL medicine, HYDROGEN peroxide, HYPERTROPHY, HYPOCHLORITES, CHINESE medicine, OXIDOREDUCTASES, PULMONARY hypertension, RATS, PLANT extracts, VENTRICULAR remodeling, IN vivo studies, DISEASE complications
Abstract

Right ventricle (RV) remodeling is a major pathological feature in pulmonary arterial hypertension (PAH). Magnesium lithospermate B (MLB) is a compound isolated from the roots of Salvia miltiorrhiza and it possesses multiple pharmacological activities such as anti-inflammation and antioxidation. This study aims to investigate whether MLB is able to prevent RV remodeling in PAH and the underlying mechanisms. In vivo , SD rats were exposed to 10% O2 for 21 d to induce RV remodeling, which showed hypertrophic features (increases in the ratio of RV weight to tibia length, cellular size, and hypertrophic marker expression), accompanied by upregulation in expression of NADPH oxidases (NOX2 and NOX4) and vascular peroxidase 1 (VPO1), increases in hydrogen peroxide (H2 O2) and hypochlorous acid (HOCl) production and elevation in phosphorylation levels of ERK; these changes were attenuated by treating rats with MLB. In vitro , the cultured H9c2 cells were exposed to 3% O2 for 24 h to induce hypertrophy, which showed hypertrophic features (increases in cellular size and hypertrophic marker expression). Administration of MLB or VAS2870 (a positive control for NOX inhibitor) could prevent cardiomyocyte hypertrophy concomitant with decreases in NOX (NOX2 and NOX4) and VPO1 expression, H2 O2 and HOCl production, and ERK phosphorylation. Based on these observations, we conclude that MLB is able to prevent RV remodeling in hypoxic PAH rats through a mechanism involving a suppression of NOX/VPO1 pathway as well as ERK signaling pathway. MLB may possess the potential clinical value for PAH therapy. [ABSTRACT FROM AUTHOR]

Published
2019
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4. Beneficial effects of capsiate on ethanol-induced mucosal injury in rats are related to stimulation of calcitonin gene-related Peptide release.

Author

Li NS, Luo XJ, Dai Z, Liu B, Zhang YS, Yang ZC, and Peng J

Subjects
Animals, Apoptosis drug effects, Capsaicin pharmacology, Capsaicin therapeutic use, Caspase 3 metabolism, Disease Models, Animal, Ethanol, Gastric Mucosa metabolism, Gastrointestinal Agents pharmacology, Gastrointestinal Agents therapeutic use, Male, Malondialdehyde blood, Plant Extracts pharmacology, Plant Extracts therapeutic use, Rats, Rats, Sprague-Dawley, Severity of Illness Index, Stomach Ulcer chemically induced, Stomach Ulcer metabolism, Superoxide Dismutase metabolism, Tumor Necrosis Factor-alpha blood, Calcitonin Gene-Related Peptide metabolism, Capsaicin analogs & derivatives, Capsicum chemistry, Gastric Mucosa drug effects, Phytotherapy, Stomach Ulcer drug therapy, TRPV Cation Channels metabolism
Abstract

Capsiate is a non-pungent analogue of capsaicin from CH-19 Sweet peppers. Capsaicin is reported to trigger calcitonin gene-related peptide (CGRP) release through activation of transient receptor potential vanilloid subfamily member 1 (TRPV1) and produces beneficial effects on gastric mucosa. This study aimed to investigate whether capsiate is able to produce beneficial effects on gastric mucosa and whether the protective effects of capsipate occur through a mechanism involving the activation of TRPV1 and CGRP release. A rat model of gastric mucosal injury was established by the oral administration of acidified ethanol. Gastric tissues were collected for analysis of the gastric ulcer index, cellular apoptosis, activities of caspase-3, catalase and superoxide dismutase (SOD), and levels of CGRP, TNF-α, and malondialdehyde (MDA). Our results show that the acute administration of ethanol significantly increased the gastric ulcer index concomitantly with an increase in cellular apoptosis, caspase-3 activity, and TNF-α and MDA levels, as well as a decrease in the activities of catalase and SOD. Pretreatment with 1 mg/kg capsiate attenuated ethanol-induced gastric mucosal injury and cellular apoptosis accompanied by an increase in CGRP level, catalase, and SOD activities, and a decrease in caspase-3 activity, and TNF-α and MDA levels. The effects of capsiate were inhibited by capsazepine, an antagonist of TRPV1. These results suggest that capsiate is able to produce beneficial effects on ethanol-induced gastric mucosal injury. These effects are related to the stimulation of CGRP release through the activation of TRPV1., (© Georg Thieme Verlag KG Stuttgart · New York.)

Published
2012
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