scholarly journals Constituents, Pharmacokinetics, and Pharmacology of Gegen-Qinlian Decoction

2021 ◽  
Vol 12 ◽  
Author(s):  
Jing-Ze Lu ◽  
Dan Ye ◽  
Bing-Liang Ma

Gegen-Qinlian decoction (GQD) is a classic traditional Chinese medicine (TCM) formula. It is composed of four TCMs, including Puerariae Lobatae Radix, Scutellariae Radix, Coptidis Rhizoma, and Glycyrrhizae Radix et Rhizoma Praeparata cum Melle. GQD is traditionally and clinically used to treat both the “external and internal symptoms” of diarrhea with fever. In this review, key words related to GQD were searched in the Web of Science, PubMed, China National Knowledge Infrastructure (CNKI), and other databases. Literature published mainly from 2000 to 2020 was screened and summarized. The main constituents of GQD could be classified into eight groups according to their structures: flavonoid C-glycosides, flavonoid O-glucuronides, benzylisoquinoline alkaloids, free flavonoids, flavonoid O-glycosides, coumarins, triterpenoid saponins, and others. The parent constituents of GQD that enter circulation mainly include puerarin and daidzein from Puerariae Lobatae Radix, baicalin and wogonoside from Scutellariae Radix, berberine and magnoflorine from Coptidis Rhizoma, as well as glycyrrhetinic acid and glycyrrhizic acid from Glycyrrhizae Radix et Rhizoma Praeparata cum Melle. GQD is effective against inflammatory intestinal diseases, including diarrhea, ulcerative colitis, and intestinal adverse reactions caused by chemotherapeutic agents. Moreover, GQD has significant effects on metabolic diseases, such as nonalcoholic fatty liver and type 2 diabetes. Furthermore, GQD can be used to treat lung injury. In brief, the main constituents, the pharmacokinetic and pharmacological profiles of GQD were summarized in this review. In addition, several issues of GQD including effective constituents, interactions between the constituents, pharmacokinetics, interaction potential with drugs and pharmacological effects were discussed, and related future researches were prospected in this review.

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Longman Li ◽  
Xiaobo Yang

Manganese (Mn) is an essential element that is involved in the synthesis and activation of many enzymes and in the regulation of the metabolism of glucose and lipids in humans. In addition, Mn is one of the required components for Mn superoxide dismutase (MnSOD) that is mainly responsible for scavenging reactive oxygen species (ROS) in mitochondrial oxidative stress. Both Mn deficiency and intoxication are associated with adverse metabolic and neuropsychiatric effects. Over the past few decades, the prevalence of metabolic diseases, including type 2 diabetes mellitus (T2MD), obesity, insulin resistance, atherosclerosis, hyperlipidemia, nonalcoholic fatty liver disease (NAFLD), and hepatic steatosis, has increased dramatically. Previous studies have found that ROS generation, oxidative stress, and inflammation are critical for the pathogenesis of metabolic diseases. In addition, deficiency in dietary Mn as well as excessive Mn exposure could increase ROS generation and result in further oxidative stress. However, the relationship between Mn and metabolic diseases is not clear. In this review, we provide insights into the role Mn plays in the prevention and development of metabolic diseases.


2021 ◽  
Vol 46 (1) ◽  
pp. 11-22
Author(s):  
Zoran Joksimović ◽  
Dušan Bastać ◽  
Snežana Pavlović

The gut microbiota of our organism is a community of bacteria, archaea, fungi, viruses and parasites that make up a unique ecosystem in the digestive tract, which consists of about 1014 microorganisms. The diversity of this community between individuals occurs because of the differences in the host genome and the impact of environmental factors, including hygiene, diet, lifestyle and the use of different drugs. Significant evidence suggests that changes in the microbiota could play a role in cardiovascular diseases. The results of research papers for the last two decades have confirmed that altered gut microbiota composition (dysbiosis) contributes to the development of various diseases, including cardiovascular diseases, type 2 diabetes, chronic kidney disease, nonalcoholic fatty liver disease, chronic inflammatory bowel disease and even certain types of cancer. There is growing evidence that in the future, apart from current predisposing factors for cardiovascular and metabolic diseases, including genetic, environmental and lifestyle factors, one should count on new risk factors such as nutritional disproportion and gut dysbiosis. Thus, we look upon the relationship between the gastrointestinal tract and cardiovascular system, i.e. the "gut-heart axis" in a new way.


2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Lili Yu ◽  
Yanhua Li ◽  
Cancan Du ◽  
Weidong Zhao ◽  
Hanxiao Zhang ◽  
...  

Obesity-induced chronic inflammation is known to promote the development of many metabolic diseases, especially insulin resistance, type 2 diabetes mellitus, nonalcoholic fatty liver disease, and atherosclerosis. Pattern recognition receptor-mediated inflammation is an important determinant for the initiation and progression of these metabolic diseases. Here, we review the major features of the current understanding with respect to obesity-related chronic inflammation in metabolic tissues, focus on Toll-like receptors and nucleotide-binding oligomerization domain-like receptors with an emphasis on how these receptors determine metabolic disease progression, and provide a summary on the development and progress of PRR antagonists for therapeutic intervention.


2021 ◽  
Vol 2 (2) ◽  
pp. 15-24
Author(s):  
Farida Mirzakarimova ◽  
◽  
Svetlana Kaleda ◽  
Natalia Polikarpova ◽  
Abdumurad Babadjanov

Nowadays, NAFLD is considered one of the leading causes of chronic liver diseases globally.This is probably becausea patient with NAFLD usually had more severe diseases -diabetes mellitus type 2 (DM-2), metabolic syndrome, etc. On the one hand, after it was established that insulin resistance underlies these metabolic diseases and, on the other hand, that compensationfor these conditions does not eliminate NAFLD, and the presence of NAFLD worsens the course of the underlying disease, interest in its study increased significantly. The development of NAFLD is increasingly associated with the hypothesis of multifactorial parallel effects, or "multiple parallel hits" ("multiple parallel hits").


2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
I. S. Stafeev ◽  
A. V. Vorotnikov ◽  
E. I. Ratner ◽  
M. Y. Menshikov ◽  
Ye. V. Parfyonova

Obesity is a growing problem in modern society and medicine. It closely associates with metabolic disorders such as type 2 diabetes mellitus (T2DM) and hepatic and cardiovascular diseases such as nonalcoholic fatty liver disease, atherosclerosis, myocarditis, and hypertension. Obesity is often associated with latent inflammation; however, the link between inflammation, obesity, T2DM, and cardiovascular diseases is still poorly understood. Insulin resistance is the earliest feature of metabolic disorders. It mostly develops as a result of dysregulated insulin signaling in insulin-sensitive cells, as compared to inactivating mutations in insulin receptor or signaling proteins that occur relatively rare. Here, we argue that inflammatory signaling provides a link between latent inflammation, obesity, insulin resistance, and metabolic disorders. We further hypothesize that insulin-activated PI3-kinase pathway and inflammatory signaling mediated by several IκB kinases may constitute negative feedback leading to insulin resistance at least in the fat tissue. Finally, we discuss perspectives for anti-inflammatory therapies in treating the metabolic diseases.


Author(s):  
Mary P Moore ◽  
Rory P Cunningham ◽  
Rachel A. H. Davis ◽  
Sarah E. Deemer ◽  
Brandon M. Roberts ◽  
...  

Nutritional ketosis as a therapeutic tool has extended to the treatment of metabolic diseases including - obesity, type 2 diabetes and nonalcoholic fatty liver disease. The purpose of this study was to determine whether dietary administration of the ketone ester (KE), R,S-1,3-butanediol diacetoacetate (BD-AcAc2), attenuates markers of hepatic stellate cell (HSC) activation and hepatic fibrosis in the context of high fat diet (HFD)-induced obesity. Six-week-old male C57BL/6J mice were placed on a 10-week ad libitum HFD (45% FAT, 32% CHO, 23% PRO). Mice were then randomized to 1 of 3 groups (n = 10 per group) for an additional 12 weeks: 1) control (CON), continuous HFD, 2) pair-fed (PF) to KE; and 3) KE (HFD+30% energy from BD-AcAc2, KE). KE feeding significantly reduced histological steatosis, inflammation and total NAFLD activity score vs CON, beyond improvements observed for calorie restriction alone (PF). Dietary KE supplementation also reduced the protein content and gene expression of pro-fibrotic markers (α-SMA, Col1a1, PDGF-β, MMP9) vs CON (p<0.05), beyond reductions observed for PF vs CON. Furthermore, KE feeding increased hepatic markers of anti-inflammatory M2 macrophages (CD163) and also reduced pro-inflammatory markers (TRAIL and CCN1) vs CON and PF (p ≤ 0.05), in the absence of changes in markers of total hepatic macrophage content (F4/80 and CD68; p > 0.05). These data highlight that the dietary ketone ester, BD-AcAc2, ameliorates histological NAFLD and inflammation and reduces pro-fibrotic and pro-inflammatory markers. Future studies to further explore potential mechanisms are warranted.


2019 ◽  
Author(s):  
Patamu Mohemaiti ◽  
Aidibai Simayi ◽  
Xiao Xiao Qin ◽  
Aizhatiguli Kadeer

Abstract Background: To investigate the effects of air pollutants on the incidence of diabetes, and to provide reliable evidence for the prevention and control of diabetes.Method: Electronic databases of PubMed, Embase, Web of Science, Wanfang Digital Periodicals (WANFANG), WeiPu, China National Knowledge Infrastructure (CNKI), Springer, and Ovid were searched. RevMan5.3 software was used for meta analysis of the literature included in this study, I2 was used to measure the heterogeneity of the research contents of the included literature, and fixed effect model or random effect model was used for combined analysis of the overall incidence of diabetes and the incidence of diabetes under different air pollutants.Result: A total of 22 articles with high overall quality were included in this study, including 2703882 subjects and 535190 patients with diabetes.Pooled effect of the studies was determined using relative risk(RR). PM10 (RR=1.00; 95%CI:0.99-1.02, P=0.61), PM2.5 (RR=1.02 ; 95%CI:1.01-1.04, P=0.01), NOX (RR=1.00; 95%CI:1.00-1.01, P=0.006), NO2 (RR=1.00; 95%CI:1.00-1.01, P=0.01), O3 (RR=1.00; 95%CI:0.99-1.01, P=0.99). No correlation was found between PM10, NO2, O3 and the risk of type 2 diabetes. The risk of diabetes increased by 1% in people exposed to total air pollutants, increased by 2% in people exposed to PM2.5, and increased by 1% in people exposed to NOX.Conclusion: Results of this paper showed that air pollutants are weakly positively correlated with the risk of diabetes. As to the other influencing factors should be further studied.


2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Ze-jun Ma ◽  
Rui Chen ◽  
Hui-Zhu Ren ◽  
Xin Guo ◽  
Jun Guo ◽  
...  

Many studies have assessed the association between eNOS-4b/a polymorphism and the risk of diabetic retinopathy (DR) among type 2 diabetic subjects. However, the results are inconsistent. In order to derive a more precise estimation of the association, a meta-analysis was conducted. Fifteen studies with 3, 183 cases and 3, 410 controls were enrolled by searching the databases of Pubmed, Embase, China National Knowledge Infrastructure (CNKI), and Chinese Wanfang Database. Summary odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. The main analysis indicated no significant association between eNOS-4b/a polymorphism and the risk of DR in overall population [allelic model:OR=0.94(0.79–1.11); additive model:OR=0.91(0.73–1.14); recessive model:OR=1.01(0.81–1.25); dominant model:OR=0.91(0.75–1.09)]. Subgroup analysis by ethnicity also indicated no significant association. In conclusion, the current meta-analysis did not observe any association between the polymorphism of eNOS 4b/a and the risk of DR among type 2 diabetic subjects. However, larger well-designed studies are required to confirm this finding.


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