Objective To explore the mechanism of Jianshen Lishui Decoction on nerve cell apoptosis in rats with cerebral hemorrhage.Methods The expression of miR-153 in cerebral hemorrhage was analyzed by miRNA microarray and RT-PCR,and the relationship between miR-153 and neuronal apoptosis in cerebral hemorrhage was observed,and predicted the target gene of miR-153;the binding of miR-153 to target genes was studied by dual-luciferase reporter gene Experiments,and to observe the effects of overexpression and inhibition of miR-153 on target genes.Subsequently,the relationship between target genes and neuronal apoptosis in cerebral hemorrhage was determined.Finally,the effect of Jianshen Lishui Decoction on miR-153 and the target gene,and finally explored the related mechanism of Jianshen Lishui Decoction on nerve cell apoptosis in rats with cerebral hemorrhage.Results Microarray chip and RT-PCR detection showed that miR-153 was lowly expressed in cerebral hemorrhage(P<0.05),and miR-153 was negatively correlated with neuronal apoptosis(R:-0.875,P=0.0002).The online databases TargetScan and miRDB showed that miR-153 has a binding region with TREM1,and the dual-luciferase reporter gene demonstrated a binding relationship between the two.When miR-153 was overexpressed,the expression of TREM1 was down-regulated,conversely,up-regulated when miR-153 was repressed,and TREM1 was positively correlated with nerve cell apoptosis(R:0.857,P<0.001).The expression of TREM1,the number of nerve cell apoptosis and the score of Neurological Deficit Scores in the Jianshen Lishui Decoction group were lower than those in the model group(P<0.05),and the expression of miR-153 was higher than that in the model group(P<0.05).The expression of TREM1,the number of nerve cell apoptosis and the score of Neurological Deficit Scores in the Jianshen Lishui Decoction +miR-153 inhibition group were higher than those in the Jianshen Lishui Decoction group(P<0.05).Conclusion Jianshen Lishui Decoction inhibits the apoptosis of nerve cells and protects the neurologicalfunctions in rats with cerebral hemorrhage by promoting miR-153 expression and inhibitingTREM1 expression.

Objective To study the effects of geniposide(Gen)on the injury of human neuroblastoma cell SH-SY5Y induced by oxygen glucose deprivation/reoxygenation(OGD/R)and its mechanism.Methods SH-SY5Y cells were divided into control group,OGD/R group,low medium and high concentration groups of Gen(12.5,25,50 μmol·L-1).Except the control group,OGD/R injury models were established in other groups,and different concentrations of Gen were used for intervention.Cell proliferation activity was detected by CCK-8 assay.The levels of lactate dehydrogenase(LDH),superoxide dismutase(SOD),malonaldehyde(MDA)and glutathione(GSH)in cell supernatant were detected by biochemical method.The intracellular Fe2+ level was detected by colorimetry.The level of reactive oxygen species(ROS)in cells was detected by flow cytometry.The protein expression levels of glutathione peroxidase 4(GPX4),solute carrier family 7 member 11(SLC7A11)and transferrin receptor 1(TFR1)in cells were detected by Western blot.Results Compared with the control group,LDH release rate,MDA content,Fe2+ level,ROS level and TFR1 expression level in OGD/R group were significantly increased(P<0.05),while cell proliferation activity,SOD activity,GSH level,SLC7A11 and GPX4 expression levels were significantly decreased(P<0.05).Compared with the OGD/R group,the LDH release rate,MDA content,Fe2+ level,ROS level and TFR1 expression level of cells in each concentration group of Gen decreased significantly(P<0.05),while cell proliferation activity,SOD activity,GSH level,SLC7A11 and GPX4 expression levels increased significantly(P<0.05),especially in H-Gen group.Conclusion Gen can inhibit oxidative stress and ferroptosis of SH-SY5Y cells induced by OGD/R,and its mechanism may be related to the activation of SLC7A11/GPX4 signal pathway.

Objective To investigate the effect of mogrol on lung injury in rats with severe acute pancreatitis and its possible mechanism.Methods The model of lung injury in rats with severe acute pancreatitis was established by retrograde injection of 4%sodium taurocholate into the biliopancreatic duct,After modeling,they were divided into model group,mogrol low,medium and high dose groups(15,30,60 mg·kg-1),set up another sham operation group,each group containing 12 rats.Intraperitoneal injection,one day once time,a total of 2 times.The pathological changes of pancreas and lung tissues were detected by HE staining;Serum amylase(AMS)and lipase(LPS)levels were detected by biochemical method;The levels of inflammatory cytokines interleukin-1β(IL-1β),interleukin-18(IL-18)and tumor necrosis factor-α(TNF-α)in rat alveolar lavage fluid were determined by ELISA;The activity of Caspase-1 in lung tissue of rats was detected by colorimetry;The expression levels of triggering receptor 1(TREM-1)and pyroptosis related proteins NLRP3,Caspasse-1,Gasdermin D(GSDMD)in lung tissue of rats were detected by Western blot.Results Compared with the sham operation group,the model group showed obvious pathological damage in pancreas and lung tissue.Serum AMS and LPS levels,inflammatory factors IL-1β,IL-18 and TNF-α levels,Caspase-1 activity,and protein expression levels of TREM-1 and NLRP3,Caspasse-1,GSDMD,in lung tissue were significantly increased(P<0.05);Compared with the model group,different doses of mogrol could improve the pathological damage of pancreas and lung tissue in rats,and significantly reduce the levels of serum AMS,LPS,inflammatory factors IL-1β,IL-18 and TNF-α,Caspase-1 activity and the expression levels of TREM-1 and NLRP3,Caspasse-1,GSDMD in lung tissue.Conclusion Mogrol may improve lung injury in rats with severe acute pancreatitis by inhibiting pyroptosis,and its mechanism may be related to the regulation of TREM-1/NLRP3 signaling pathway.

Dendrobium is one of the valuable Chinese herbs in China,and Dendrobium officinale is the top grade of Dendrobium,which is recorded in many ancient medical texts as having the efficacy of treating diabetes.Modern pharmacological research shows that Dendrobium has the effects of anti-tumor,anti-fatigue,immune regulation,anti-aging,and regulation of glycolipid metabolism.In clinical application,Dendrobium officinale also has the function of balancing glucose and lipid metabolism,improving insulin resistance,promoting insulin secretion,improving the function of islet cells,and has a certain role in the prevention and treatment of diabetic complications.At present,there is a lack of systematic review of the pharmacological mechanism of Dendrobium officinale in the treatment of diabetes.In order to understand the pharmacological action of Dendrobium officinale in the treatment of diabetes more comprehensively,and to provide a reference for further pharmacological research,so that it can be better applied in clinics,this paper reviews the research progress of the pharmacological mechanism of Dendrobium officinale in the treatment of diabetes.

Ulcerative colitis is a chronic,non-specific inflammatory disease.The persistent damage to its intestinal epithelium is key to the development of the disease.In recent years,a new form of cell death has been identified by researchers-iron death-which is thought to be an important contributor to intestinal epithelial cell death.The occurrence of iron death is often associated with abnormal intracellular iron metabolism,reduced cystine/glutamate reverse transporter activity,abnormal lipid metabolism,voltage-dependent anion channel activation and overexpression of the Nrf2 gene.Iron death can lead to smaller mitochondria,increased membrane density and reduced number of cristae,unlike conventional cell death,which does not exhibit specific phenomena.Studies have found that TCM can alleviate iron death in intestinal epithelial cells by reducing intracellular iron content,inhibiting lipid reactive oxygen species production and regulating Nrf2 gene expression,thus acting as a treatment for ulcerative colitis.Therefore,Chinese medicine may become an important tool for the treatment of ulcerative colitis.This paper reviews the relationship between cellular iron death and ulcerative colitis and the research progress of Chinese medicine in treating ulcerative colitis through the iron death pathway.

Discipline construction is the power source to realize the high quality development of public hospitals,and high quality scientific research management is the inevitable path to realize the connotative development of public hospitals.The quality improvement of scientific research project process management is step-by-step,and mid-term inspection is a representative work.This paper applies PDCA cycle theory to the mid-term inspection of scientific research projects,analyzes the problems encountered in the mid-term inspection of scientific research projects from the four stages of plan,implementation,check and act,and develops effective intervention measures.The mid-term inspection mode,which combines publicity activities of scientific research norms with self-examination by researchers and on-the-spot inspection by the scientific research department,should be carried out to standardize the process of mid-term inspection of scientific research projects and promote the high-quality development of scientific research in hospitals.

As population aging progresses,musculoskeletal health will serve as one of the most important indicators of health status in older adults.Studies related to the promotion of vitamin D absorption by drugs are now more common,but the drugs are accompanied by subsequent side effects.Notably,several non-pharmacological therapies are also being investigated for their respective effects on promoting vitamin D absorption.The purpose of this paper is to analyze the mechanism of vitamin D in osteoporosis,and to discuss the progress of research on the promotion of vitamin D absorption by acupuncture,tui na and acupuncture point burial,as well as by sunlight,diet,aerobic exercise,tai chi and aerobics,in order to provide a reference for clinical and scientific research on the selection of appropriate methods to promote vitamin D absorption.At the same time,it provides a non-pharmacological way to control bone loss for people with long-term home bone loss and osteoporosis.

In recent years,with the development of the bio-psycho-social medical model,more and more attention has been paid to the relationship between psycho-emotional factors and liver.According to traditional Chinese medicine theory,the liver is mainly responsible for catharsis and regulating emotion,which is closely related to emotion.Epidemiological studies have shown that all kinds of liver diseases are accompanied by different degrees of mental disorders,and mental and emotional abnormalities may promote the occurrence of liver diseases and affect the prognosis.Liver and emotion have a common pathogenesis in pathology,involving the dysfunction of nervous,endocrine and immune systems.Based on the basic theory of traditional Chinese medicine and modern medical research,this review analyzes the correlation between emotions and liver.At the same time,neurotransmitters,inflammatory cytokines,brain-derived neurotrophic factor(BDNF),soluble epoxide hydrolase(sEH),intestinal microecology,hypothalamic-pituitary-adrenal(HPA)axis and hypothalamic-pituitary-thyroid(HPT)axis,which summarizes the potential mechanisms of liver disease complicated with emotional disorders,and provides certain reference value for future theoretical research and clinical treatment.

The senescence accelerate mouse prone are a model of early learning and memory impairment,because they exhibit most of the characteristics of the pathogenesis of Alzheimer's disease,including abnormal expression of anti-aging factors,excessive increase of inflammatory factors,amyloid deposition,tau protein hyperphosphorylation,mitochondrial autophagy,the central mechanism of blood-brain barrier damage,and pathological damage of multiple systems and organs.Therefore,it has been widely used as an ideal model for Alzheimer's disease research.With the deepening of the experimental research on the mechanism of AD,it was found that SAMP8 mice showed obvious changes in behavior,histopathology and biochemical parameters compared with SAMR1,which were similar to human diseases.Therefore,this paper reviews the research progress of SAMP8 mice in recent years,in order to provide useful guidance and help for the application of SAMP8 mouse model in a variety of aging diseases.

Body fluid refers to all normal fluids in the human body,which are the basic substances that constitute human tissues and organs.It is also an essential foundation for maintaining normal life activities of the body.Its abnormal evolution in the human body is highly consistent with the pathological changes of dementia.This paper combs the internal relationship between normal body fluid metabolism and healthy human cognitive function,analyzes the corresponding relationship between the viscera related to regulating body fluid metabolism and the evolution of body fluid pathological changes and the degenerative pathological evolution of dementia from the natural aging time axis,emphasizes that the body fluid metabolism disorder is the core pathogenesis of dementia.We believe that in the early stages,preventive and conditioning methods such as a balanced diet and regular living habits should be implemented;In the mid-term stage,the focus is on regulating the Pi circulation and dialectical medication;In the later stage,on the basis of strengthening Pi circulation,it is necessary to support the diseased organs and treat them according to relevant syndromes.