Context: Rhizoma Corydalis (RC) is the dried tubers of Corydalis yanhusuo (Y. H. Chou and Chun C. Hsu) W. T. Wang ex Z. Y. Su and C. Y. Wu (Papaveraceae). Traditionally, RC is used to alleviate pain such as headache, abdominal pain, and epigastric pain. Modern medicine shows that it has analgesic, antiarrhythmia, and other effects. Objective: We provided an overview of the phytochemical and pharmacological properties of RC as a foundation for its clinical application and further research and development of new drugs. Methods: We collected data of various phytochemical and pharmacological effects of RC from 1982 to 2019. To correlate with existing scientific evidence, we used Google Scholar and the journal databases Scopus, PubMed, and CNKI. 'Rhizoma Corydalis', 'phytochemistry', and 'pharmacological effects' were used as key words. Results: Currently, more than 100 chemical components have been isolated and identified from RC, among which alkaloid is the pimary active component of RC. Based on prior research, RC has antinociceptive, sedative, anti-epileptic, antidepressive and anti-anxiety, acetylcholinesterase inhibitory effect, drug abstinence, anti-arrhythmic, antimyocardial infarction, dilated coronary artery, cerebral ischaemia reperfusion (I/R) injury protection, antihypertensive, antithrombotic, antigastrointestinal ulcer, liver protection, antimicrobial, anti-inflammation, antiviral, and anticancer effects. Conclusions: RC is reported to be effective in treating a variety of diseases. Current pharmacological studies on RC mainly focus on the nervous, circulatory, digestive, and endocrine systems, as well as drug withdrawal. Although experimental data support the beneficial effects of this drug, its physiological activity remains a concern. Nonetheless, this review provides a foundation for future research.
To investigate the characteristics of diabetic patients with foot ulcers, their health-related quality of life (HRQoL), and the link between them. The study population included 131 consecutive patients presenting in a diabetic foot clinic with a new foot ulcer between December 1, 2011, and May 1, 2012. The authors collected sociodemographic data, foot and ulcer characteristics using the Wagner Grade, and HRQoL (using the SF-36 Scale) information; 54.2% of the patients were in Wagner 2 or Wagner 3 categories. In all the 8 SF-36 subscales and in the SF-36 summary scales, the patients with diabetic foot ulcer had significantly poorer HRQoL than the general population in China (P < .01). Their Wagner Grade had negative correlation with all the SF-36 subscales and the summary scales (P < .05). In conclusion, new diabetic foot ulcers were already in poor condition when patients first visited the diabetic foot clinic. Concomitantly, patients had worse HRQoL compared with the general population. More effective interventions are needed to improve their self-care level and HRQoL.
Dermatological problems in diabetes might play an important role in the spontaneous ulcers and impaired wound healing that are seen in diabetic patients. Investigation of the cause of diabetic skin disorders is critical for identifying effective treatment. The abdominal full-thickness skin tissues of 33 patients (14 nondiabetic and 19 diabetic) were analyzed. The cell viability and malondialdehyde (MDA) production of fibroblasts were measured after advanced glycosylation end product (AGE)-bovine serum albumin (BSA) exposure. Cutaneous histological observation showed reduced thickness of the diabetic abdominal dermis with morphological characteristics of obscured multilayer epithelium and shortened, thinned, and disorganized collagen fibrils with focal chronic inflammatory cell infiltration when compared with controls of the same age. Accumulation of AGEs in diabetic skin was prominent. Less hydroxyproline, higher myeloperoxidase activity, and increased MDA content were detected in diabetic skin. In vitro, the time- and dose-dependent inhibitory effects of AGE-BSA on fibroblast viability as well as the fact that AGE-BSA could promote MDA production of fibroblasts were shown. It is shown that the accumulation of AGEs in diabetic skin tissue induces an oxidative damage of fibroblasts and acts as an important contributor to the thinner diabetic abdominal dermis. The authors believe that diabetic cutaneous properties at baseline may increase the susceptibility to injury, and diabetic wounds possess atypical origin in the repair process.
Inflammation, initiated by polymorphonuclear neutrophil (PMNs) infiltration, is the first step in wound healing. The aim of this study is to investigate the function of neutrophils in a diabetes-impaired wound healing model and to explore the underlying mechanisms leading to neutrophil dysfunction. Superficial second-degree burns were created in the streptozotocin (STZ)-induced diabetic rat model, and the changes in the levels of advanced glycation end products (AGE), receptor of AGE (RAGE), inflammatory cytokines and oxidative markers, as well as cell apoptosis were determined. The effects of AGE on isolated PMNs were also determined in vitro. We found that deposition of AGE in diabetic rat skin activated the neutrophils before injury. However, the dense inflammatory band failed to form in the diabetic rats after injury. Compared with the controls, enhanced expression of RAGE and accelerated cell apoptosis were observed in the burned skin of diabetic rats. The altered expression pattern of inflammatory cytokines (tumor necrosis factor-alpha and interleukin-8) and oxidative markers (glutathione peroxidase, myeloperoxidase, hydrogen peroxide, and malondialdehyde) between burned skin of diabetic and control rats revealed delayed neutrophil chemotaxis and respiratory burst. Furthermore, the results in vitro showed that exposure to AGE inhibited the viability of PMNs, promoted RAGE production and cell apoptosis, and prevented the migration of PMNs, consistent with the findings in vivo. Besides, AGE-treated neutrophils showed increased secretion of inflammatory cytokines and increased oxidative stress. Combined, our results suggest that an interaction between AGE and its receptors inhibits neutrophil viability and function in the diabetic rat burn model.
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