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ObjectiveTo explore the possible mechanism of Pingwei Capsules （平胃胶囊） for chronic atrophic gastritis from rapidly accelerated fibrosarcoma / mitogen-activated protein kinase /extracellular-signal-regulated kinase （Raf/MEK/ERK） pathway that influences the activation of fibrosarcoma protein/mitogen. MethodsFifteen SD rats were randomly divided into 5 rats in the blank group and 10 rats in Pingwei Capsules group. The rats in the blank group were given 1 ml/100 g of saline by gavage， and the rats in Pingwei Capsules group were given 0.63 g/（kg·d） of Pingwei Capsule suspension by gavage， and serum was collected for 3 consecutive days. N-methyl-N'-nitro-N-nitrosoguanidine （MNNG） was used to induce human gastric mucosal epithelial cells GES-1 to establish a precancerous lesion cell model. The successful cells were divided into control group （10% fetal bovine serum）， blank serum group （10% fetal bovine serum plus 10% blank serum）， and medication-containing serum group （serum with medication of Pingwei Capsule）， and the volume fraction and time of intervention of Pingwei Capsule-containing serum were screened by CCK-8 assay. Human gastric mucosal epithelial cells GES-1 were divided into normal group， model group， blank serum group， medication-containing serum group， U0126 group， and combined group， with 6 replicate wells in each group. After successful modelling of the cells in all groups except the blank group， an equal volume of fetal bovine serum was added to the normal and model groups， an equal volume of blank serum was added to the blank serum group， a screening volume fraction of Pingwei Capsule-containing serum was added to Pingwei Capsule group， a 10 μmol/L mitogen-activated extracellular signal regulated kinase 1 （MEK1） inhibitor U0126 was administered in the U0126 group， an equal dose of Pingwei Capsule-containing serum plus 10 μmol/L of U0126 was administered to the combined group. After the selected incubation time， the level of interleukin 6 （IL-6） was detected in the cells by ELISA， the expression of IL-6 and MEK1 was detected by immunofluorescence， and the expression of IL-6， Raf， MEK1， and ERK mRNA was detected by RT-qPCR， and the expression of IL-6， Raf， MEK1， and ERK mRNA in the cells was detected by Western blot. ResultsThe 5.35% volume fraction， 48 h intervention of Pingwei Capsule-containing serum was selected for subsequent experiments. Compared with the normal group， the IL-6 content in cell supernatants and the expression of IL-6， Raf， MEK1， ERK mRNA and ERK1/2 proteins in cells increased in the model group and blank serum group （P＜0.01）. Compared with the model group， all of the above indexes were improved in medication-containing serum group， U0126 group， and combined group （P＜0.05 or P＜0.01）. Compared with medication-containing serum group， the expression of IL-6， MEK1 expression， the expression of IL-6， Raf， MEK1 and ERK mRNA， and the expression of IL-6， Raf， MEK1 and ERK1/2 proteins reduced in the cells of combined group （P＜0.05 or P＜0.01）. Compared with the U0126 group， IL-6 expression reduced and IL-6， MEK1 and ERK1/2 protein expression reduced in cells of combined group （P＜0.05 or P＜0.01）. ConclusionThe Pingwei Capsule-containing serum may play a role in the treatment of chronic atrophic gastritis by improving the inflammation-cancer transformation of GES-1 cells through inhibiting the Raf/MEK/ERK pathway.
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Based on the method of regulating qi and resolving toxins， this paper discussed the core pathogenesis of “inflammation-cancer” transformation of ulcerative colitis. It is believed that the disorder of qi movement， endogenous pathogenic factors of “heat， stasis and dampness” are cemented in the large intestine， and the pathogenic factors are too excessive to be solved， which will become toxic after a long time and lead to cancerous changes. Clinical prevention and treatment applies the method of regulating qi and resolving toxins， and the method of regulating qi was proposed as clearing internal qi， regulating blood qi and strengthening spleen qi， so as to clear heat， dissipate blood stasis and dissolve dampness； different methods of regulating qi and resolving toxins were flexibly combined according to the pathogenic characteristics of different stages of toxicity， in order to interrupt the process of “inflammation-cancer” transformation of ulcerative colitis.
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As the pace of society increases and lifestyles change， the incidence and mortality rates of breast cancer continue to rise. Targeted therapies are now promising in the treatment of breast cancer， and a variety of protein targets have been identified to play an important role in the development of breast cancer. Among them， signal transducer and activator of transcription （STAT） proteins constitute a crucial group that serves as important targets for transducing cellular transcriptional information， which can regulate downstream cell proliferation， apoptosis， cell migration， invasion， angiogenic factors， etc. and then affect the progression of breast cancer. The STAT family is closely associated with the inflammatory response to tumors and plays a landmark role in tumor development as well as in diagnosis and prognosis. The "inflammation-cancer" transformation refers to the process in which the inflammatory microenvironment caused by uncontrolled inflammation promotes normal cells to become cancerous. According to the theory of Chinese medicine， "heat toxicity" in "cancer toxicity" corresponds to inflammation， which is closely related to tumor development. As a major link associated with the inflammatory response， the STAT family has a promising role in the development and treatment of a variety of tumors， but its relevance to breast cancer remains inadequately explored. Chinese medicine has been shown to have good efficacy in the prevention and treatment of breast cancer， and some current studies have shown that the active ingredients and compounds of Chinese medicine have certain intervention effects on breast cancer-related STAT proteins， but there has not been a systematic review. In order to better sort out and summarize the studies on the effects of Chinese herbal medicines based on the STAT family interventions in breast cancer， this paper reviewed the studies on Chinese herbal medicines acting on the STAT family in recent years， aiming to provide new ideas for clinical applications in breast cancer and to provide thoughts for the development of STAT protein-based drugs.
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Chronic obstructive pneumonia cancer transformation refers to the malignant transformation of long-term repeated chronic inflammation of the lung. Traditional Chinese Medicine believes that the etiology and pathogenesis of chronic obstructive pneumonia cancer transformation always belong to the deficiency of origin and excess of signs. Chronic obstructive pulmonary disease causes damage to the qi of the lung, spleen and kidney. Qi is yang, and qi deficiency leads to yang deficiency. Yang deficiency and abnormal warm would result in qi stagnation, phlegm coagulation and blood stasis. It is the key to the transformation of chronic obstructive pneumonia cancer. Kidney yang is the root of yang qi. Deficiency of kidney yang is the initiating factor for the transformation of chronic obstructive pneumonia cancer. Deficiency of lung yang is the fundamental factor for the transformation of chronic obstructive pneumonia cancer. Deficiency of kidney yang and deficiency of spleen yang are the driving factors for the transformation of chronic obstructive pneumonia cancer. Therefore, this article discussed the role of kidney yang in the transformation of chronic obstructive pneumonia cancer from the theory of "Qi Zhu Xu Zhi", in order to broaden the thinking of clinical diagnosis and treatment of the disease.
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Gastric ''inflammation-cancer'' transformation stars from inflammation and ends as gastric cancer （GC）， and the pathogenesis is still unclear. In China， GC features high morbidity and mortality and poor prognosis， influencing the quality of life and physical and mental health of patients. Therefore， it is of great significance to construct the prevention and treatment system for GC. Chronic atrophic gastritis （CAG） plays a key role in the occurrence， development， and outcome of gastric ''inflammation-cancer'' transformation. Modern therapies for CAG generally aim at eliminating causes and alleviating clinical symptoms， which show satisfactory short-term efficacy， but the reverse and recurrence are common. Based on the holistic view， syndrome differentiation-based treatment， and the ''inflammation-cancer'' transformation in modern medicine， traditional Chinese medicine emphasizes both prevention and treatment， with individualized therapies for CAG and GC to control the transformation. According to the pathogenesis of CAG-asthenia in origin and sthenia in superficiality and deficiency-excess in complexity， this study proposed the theory of spleen deficiency and pathogen stagnation in CAG， and believed spleen deficiency， pathogen， and stagnation are respectively the root cause of， the main factor of， and the key to ''inflammation-cancer'' transformation， respectively. Spleen deficiency and pathogen stagnation are closely related to the process of the transformation. For the treatment， the spleen-invigorating and pathogen-eliminating method should be used for invigorating the spleen to consolidate original Qi， improve the blood supply in stomach， and regulate immunity， and eliminating the pathogen to relieve stagnation， reduce the occurrence of non-controllable inflammation， and improve inflammatory micro-environment. As a result， the gastric inflammation is controlled at the early stage and the gastric ''inflammation-cancer'' transformation is blocked. The gastric mucosal lesions are blocked， delayed， or even reversed. This study provides a new idea in clinical diagnosis and treatment of CAG and in the prevention of GC.
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Introducción: Los ácidos biliares en condiciones no fisiológicas se consideran agentes inflamatorio-carcinógenos endógenos que originan alteraciones en membranas plasmáticas, mitocondrias, el ADN, los genes y, la apoptosis de las células epiteliales. Objetivo: Describir la asociación entre los niveles elevados de ácidos biliares en la luz intestinal y la secuencia inflamación-cáncer, expresados como lesiones inflamatorias, premalignas y malignas del tracto digestivo. Métodos: Revisión sistemática y crítica de las evidencias sobre los mecanismos biomoleculares asociados a niveles altos de ácidos biliares en la luz intestinal y la secuencia inflamación-carcinogénesis, en bases de datos como PubMed, Medline, SciELO, LILACS y Elsevier, publicados entre 2015-2020, que establecen el fundamento teórico y metabolómico de dicha secuencia. Resultados: Los ácidos biliares tienen una acción tóxica en la secuencia inflamación-cáncer del tracto digestivo, al perderse el control de su homeostasis o la integridad anatomo-funcional del sistema hepato-vesículo-bilio-intestinal. Conclusiones: Los mecanismos celulares y biomoleculares desencadenados por los niveles altos de ácidos biliares contextualizan la génesis del proceso secuencial inflamación-cáncer y su interacción con los factores de riesgo clásicos, genéticos y epigenéticos reconocidos como un nuevo paradigma fisiopatológico del cáncer digestivo(AU)
Introduction: In non-physiological conditions, bile acids (BA) are considered to be endogenous inflammatory-carcinogenic agents causing alterations in plasma membranes, mitochondria, DNA, genes and epithelial cell apoptosis. Objective: Describe the association between high bile acid levels in the intestinal lumen and the inflammation-cancer sequence, expressed as inflammatory premalignant and malignant lesions of the digestive tract. Methods: A systematic critical review was conducted of the evidence about biomolecular mechanisms associated to high bile acid levels in the intestinal lumen and the inflammation-carcinogenesis sequence published in the databases PubMed, Medline, SciELO, LILACS and Elsevier in the period 2015-2020, laying the theoretical and metabolomic foundations of that sequence. Results: Bile acids display toxic activity in the inflammation-cancer sequence of the digestive tract, since control is lost of its homeostasis or the anatomical-functional integrity of the hepato-vesicular-biliary-intestinal system. Conclusions: The cellular and biomolecular mechanisms triggered by high bile acid levels provide a context for the genesis of the inflammation-cancer sequential process and its interaction with the classic, genetic and epigenetic risk factors recognized as a new pathophysiological paradigm of digestive cancer(AU)