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Objective. The therapeutic effect of drugs for functional dyspepsia (FD) is still limited. Ganoderic acid A (GAA) has anti-inflammatory and cellular protective activities. The aim of this study is to explore the therapeutic effect of GAA on FD. Methods. The FD rat model was established via tail damping and forced exercise fatigue. The gastric emptying rate and intestinal propulsion rate of the rats in each group were then detected, and the pathological damage of gastric antrum and duodenum tissues was observed by hematoxylin-eosin (HE) staining. An enzyme-linked immunosorbent assay (ELISA) was conducted to determine the levels of motilin (MTL), vasoactive intestinal peptide (VIP), leptin, gastrin (GAS), calcitonin gene-related peptide (CGRP), and somatostatin (SS) in plasma, and Western blot was used to detect the protein expression levels of occludin, zonula occluden-1 (ZO-1), and junctional adhesion molecule-1 (JAM-1) in the duodenal tissue. Results. Treatment with GAA significantly raised the gastric emptying rate and intestinal propulsion rate of FD rats and histologically alleviated the gastric and duodenal damage. Meanwhile, GAA positively regulated the secretion of brain-gut proteins, such as upregulation of MTL, GAS, and SS and downregulation of VIP, leptin, and CGRP. In addition, GAA treatment increased the protein expression levels of occludin, ZO-1, and JAM-1 in the duodenal tissue of the FD rats. Conclusion. GAA may exhibit protective effects on FD by regulating the secretion of brain-gut peptide, protecting the intestinal barrier and improving gastrointestinal motility. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease (COPD) is a common respiratory disease with high morbidity and mortality. The conventional therapies remain palliative and have various undesired effects. Flavonoids from traditional Chinese medicine (TCM) have been proved to exert protective effects on COPD. This review aims to illuminate the poly-pharmacological properties of flavonoids in treating COPD based on laboratory evidences and clinical data and points out possible molecular mechanisms. Animal/laboratory studies and randomised clinical trials about administration of flavonoids from TCM for treating COPD from January 2010 to October 2020 were identified and collected, with the following terms: chronic obstructive pulmonary disease or chronic respiratory disease or inflammatory lung disease, and flavonoid or nature product or traditional Chinese medicine. Pharmacokinetic studies and external application treatment were excluded. A total of 15 flavonoid compounds were listed. Flavonoids could inhibit inflammation, oxidative stress, and cellular senescence, restore corticosteroid sensitivity, improve pulmonary histology, and boost pulmonary function through regulating multiple targets and signaling pathways, which manifest that flavonoids are a group of promising natural products for COPD. Nevertheless, most studies remain in the research phase of animal testing, and further clinical applications should be carried out. [ABSTRACT FROM AUTHOR]

Background. Previous studies proved that AS-IV could prevent blood-brain barrier (BBB) against an increase in permeability. However, its underlying molecular mechanism has not been enlightened yet. The aim of the study is to reveal the potential protective mechanism of astragaloside IV (AS-IV) on the blood-brain barrier after ischemia-reperfusion. Methods. In vivo, AS-IV neurological protection was measured by Long's five-point scale and 2,3,5-triphenyltetrazolium chloride staining. AS-IV protection for BBB was observed by Evans blue extravasation technique. Endoplasmic reticulum stress and apoptosis-related protein levels were measured by western blot with AS-IV intervention. In vitro, cell apoptosis was analyzed by western blot and flow cytometry.Endoplasmic reticulum stress-related protein levels were quantified through western blot. Results. AS-IV treatment could decrease the infarct size in rats' brain and protect the BBB against Evans blue permeating through brain, after ischemia/reperfusion, significantly. Further, ischemia/reperfusion or oxygen‐glucose deprivation/reperfusion was found to have an increase in endothelial cell apoptosis proteins, such as Bax, Bcl-2, and caspase-3, and endoplasmic reticulum stress-associated proteins, such as phosphorylated PERK and eIF2α, Bip, and CHOP, which were attenuated by AS-IV treatment. Conclusions. AS-IV can effectively protect the blood-brain barrier and reduce the area of cerebral infarction via inhibiting endoplasmic reticulum stress-mediated apoptosis in endothelial cells. [ABSTRACT FROM AUTHOR]

Background. Ulcerative colitis (UC) is a chronic recurrent inflammation of the colon, and clinical outcome of UC is still unsatisfied. Pingkui enema, a traditional Chinese medicine prescription, has been safely applied for the treatment of diarrhea and dysentery in clinic for many years. However, its mechanism is still elusive. The present study is designed to investigate the effect of Pingkui enema on trinitrobenzene sulfonic acid- (TNBS-) induced ulcerative colitis (UC) and possible mechanism in rats. Methods. UC was induced by intracolonic instillation of TNBS in male Sprague-Dawley rats, which were treated with different dosages of Pingkui enema (low, medium, and high) or sulfasalazine for ten days. Survival rate was calculated. A clinical disease activity score was evaluated. Histological colitis severity was analyzed by hematoxylin-eosin (HE) staining. Content of Bifidobacterium in intestinal tissue was analyzed by RT-PCR. Concentration of IL-8, IL-13, TNF-α, D-lactic acid (D-LA), and diamine oxidase (DAO) in serum and contents of adhesin and receptor of Bifidobacterium adhesion in rat intestinal mucus were measured by ELISA. Results. The results showed that Pingkui enema treatment with high dosage markedly improved the survival rate compared with untreated and sulfasalazine treated groups. All dosages of Pingkui enema reduced pathological score. High dosage of Pingkui enema and sulfasalazine treatments significantly reduced the serum concentration of IL-8, TNF-α, D-LA, and DAO and markedly increased the serum concentration of IL-13. In addition, high-dose Pingkui enema and sulfasalazine treatments increased gut content of Bifidobacterium, gut mucus expressions of adhesin, and adhesin receptor of Bifidobacterium. Conclusions. Pingkui enema has therapeutic effect on TNBS-induced UC, and possible mechanism may be via regulation of gut probiotics (Bifidobacterium) and inflammatory factors and protection of intestinal mucosal barrier. [ABSTRACT FROM AUTHOR]

Xihuang pill (XH) is a complementary and alternative medicine that has been used in traditional Chinese medicine (TCM) for the treatment of tumors since the 18th century. XH has clinical effects on non-Hodgkin lymphoma, breast cancer, gastric cancer, liver cancer, and bone metastasis. XH can also inhibit the growth of tumor cells and cancer stem cells, prevent tumor invasion and angiogenesis, and regulate the tumor microenvironment. XH is composed of Ru Xiang (olibanum), Mo Yao (Commiphora myrrha), She Xiang (Moschus), and Niu Huang (Calculus bovis). Some of the compounds found in these ingredients exert multiple antitumor effects and may synergize with the other ingredients. We aimed to summarize the clinical applications and molecular mechanisms of XH and its chemical composition. This review will provide potential new strategies and alternative perspectives for tumor treatments and basic research into complementary and alternative medicine. [ABSTRACT FROM AUTHOR]

Objective. To investigate the treatment effect and treatment length of Chinese herbal decoction (CHD) as maintenance therapy on patients with extensive-stage small-cell lung cancer (ES-SCLC) and to reflect the real syndrome differentiation (Bian Zheng) practices of traditional Chinese medicine (TCM). Patients and Methods. Different CHDs were prescribed for each patient based on syndrome differentiation. The length of CHD treatment was divided into two phases for analyzing progression-free survival (PFS) and postprogression survival (PPS). Results. Three hundred and fifty-seven CHDs were prescribed based on syndrome differentiation during the study period. Median PFS was significantly longer in patients who received CHD >3 months than patients who received CHD ≤3 months in the first phase (8.7 months versus 4.5 months; hazard ratio (HR), 0.52; 95% confidence interval (CI), 0.41–0.99; P=0.0009). Median PPS was significantly longer in patients who received CHD >7 months than patients who received CHD ≤7 months in the second phase (11.7 months versus 5.1 months; HR, 2.32; 95% CI, 1.90–2.74; P=0.002). Conclusion. CHD could improve PFS and PPS, which are closely related to treatment time and deepness of response of first-line therapy. In addition, CHD could improve body function and keep patients in a relatively stable state. [ABSTRACT FROM AUTHOR]

The new methods of different administration times for the treatment of primary dysmenorrhea are more widely used clinically; however, no obvious mechanism has been reported. Therefore, an animal model which is closer to clinical evaluation is indispensable. A novel animal experiment with different administration times, based on the mice oestrous cycle, for primary dysmenorrhoea treatment was explored in this study. Mice were randomly divided into two parts (one-cycle and three-cycle part) and each part includes five groups (12 mice per group), namely, Jingqian Zhitong Fang (JQF) 6-day group, JQF last 3-day group, Yuanhu Zhitong tablet group, model control group, and normal control group. According to the one-way ANOVAs, results (writhing reaction, and PGF2α, PGE2, NO, and calcium ions analysis by ELISA) of the JQF cycle group were in accordance with those of JQF last 3-day group. Similarly, results of three-cycle continuous administration were consistent with those of one-cycle treatment. In conclusion, the consistency of the experimental results illustrated that the novel animal model based on mice oestrous cycle with different administration times is more reasonable and feasible and can be used to explore in-depth mechanism of drugs for the treatment of primary dysmenorrhoea in future. [ABSTRACT FROM AUTHOR]