ABSTRACT
Chronic kidney disease (CKD) refers to abnormal renal structure and function for more than 3 months, and is characterized by abnormal urine, blood and kidney structure. As an important clinical manifestation of CKD, proteinuria is closely related to glomerular damage. It is not only a pathological manifestation of CKD, but also an important pathological factor to accelerate the development of CKD. After thousands of years of development, traditional Chinese medicine (TCM) has a systematic theoretical foundation and rich clinical experience in the treatment of CKD. By referring to the treatment principles and methods of "leakage of vital essence", "low back pain", "asthenia", "blood urine" and "edema" in TCM, the general treatment principle of proteinuria is to coordinate the body Yin and Yang and restore the balance of Yin and Yang. Specific methods include removing blood stasis, sweating, urinating, invigorating the spleen and strengthening the kidney, smoothing liver and activating collaterals, and removing dampness and detoxification. Both ancient and modern physicians have established effective prescriptions according to the treatment principles and methods. Modern studies have showed that the mechanism of TCM to reduce proteinuria is mainly to improve the pathological manifestations of large area fusion of podocyte processes and complete disappearance of poddout, up-regulate the expression of nephrin and podocin, regulate immune, alleviate systemic inflammation, and improve the serum superoxide dismutase (SOD)level and the ability of the body to remove free radicals. The method and mechanism of treating renal proteinuria are discussed from three aspects:classical prescriptions, empirical prescriptions and the Chinese patent medicine. It provides a theoretical reference for the clinical treatment of chronic kidney disease, reducing the excretion of proteinuria and improving the clinical symptoms of the patients.
ABSTRACT
AIM:To observe the antiulcer effect of butyric acid and hydrogen , the main metabolites of Clos-tridium butyricum (C.butyricum), and to explore the underlying mechanism .METHODS: The mouse model of acute gastric mucosal lesion was prepared by gavage with ethanol .The mice were randomly divided into 4 groups:normal group , model group , butyric acid group and hydrogen group .The mice in butyric acid group and hydrogen group were given buty-rate and hydrogen prior to model establishment , respectively .Macroscopic observation of the pathological changes in gastric tissues was performed to evaluate the effect of the 2 metabolites of C.butyricum.Meanwhile, the mRNA expression levels of inflammatory factors, such as IL-12, RAN1 and MCP-1, were determined by RT-qPCR.The expression levels of apopto-sis-related proteins Bcl-2 and Bax were detected by immunohistochemical staining .RESULTS:The macroscopic observa-tion found that butyrate , not hydrogen , protected gastric mucosa .HE staining also showed that butyrate significantly attenu-ated the pathological damage of the gastric mucosa induced by ethanol .Compared with model group , the mRNA levels of inflammatory factors IL-12, RAN1 and MCP-1 in butyrate group significantly decreased (P<0.01).In butyrate group, the protein level of Bax was obviously decreased compared with model group (P<0.01), while the protein level of Bcl-2 was significantly increased ( P<0.01 ) .CONCLUSION: The gastric mucosa protective metabolite of C.butyricum may be butyric acid , not hydrogen .Butyric acid protects the gastric mucosa against ethanol-induced lesion by inhibiting the inflam- mation and reducing the expression ratio of Bax/Bcl-2.
ABSTRACT
AIM:To observe the antiulcer effect of butyric acid and hydrogen , the main metabolites of Clos-tridium butyricum (C.butyricum), and to explore the underlying mechanism .METHODS: The mouse model of acute gastric mucosal lesion was prepared by gavage with ethanol .The mice were randomly divided into 4 groups:normal group , model group , butyric acid group and hydrogen group .The mice in butyric acid group and hydrogen group were given buty-rate and hydrogen prior to model establishment , respectively .Macroscopic observation of the pathological changes in gastric tissues was performed to evaluate the effect of the 2 metabolites of C.butyricum.Meanwhile, the mRNA expression levels of inflammatory factors, such as IL-12, RAN1 and MCP-1, were determined by RT-qPCR.The expression levels of apopto-sis-related proteins Bcl-2 and Bax were detected by immunohistochemical staining .RESULTS:The macroscopic observa-tion found that butyrate , not hydrogen , protected gastric mucosa .HE staining also showed that butyrate significantly attenu-ated the pathological damage of the gastric mucosa induced by ethanol .Compared with model group , the mRNA levels of inflammatory factors IL-12, RAN1 and MCP-1 in butyrate group significantly decreased (P<0.01).In butyrate group, the protein level of Bax was obviously decreased compared with model group (P<0.01), while the protein level of Bcl-2 was significantly increased ( P<0.01 ) .CONCLUSION: The gastric mucosa protective metabolite of C.butyricum may be butyric acid , not hydrogen .Butyric acid protects the gastric mucosa against ethanol-induced lesion by inhibiting the inflam- mation and reducing the expression ratio of Bax/Bcl-2.