Objective To observe the clinical curative effect of tripterygium polyglycoside combined with cozaar in elderly patients with IgA nephropathy (IgAN) and its influence on expressions of TGF-β1,PAI-1 and VEGF.Methods Eighty elderly patients with IgA nephropathy in Jiaxing Hospital of Armed Police Zhejiang Corps from April 2011 to January 2016 were selected and randomly divided into the control group and observation group,40 cases in each group.The two groups received the routine treatment of chronic basic diseases and took oral cozaar.On this basis the observation group took tripterygium polyglycoside for continuous 12 months.Urine protein,serum creatinine (Scr),blood urea nitrogen (BUN),plasma Alb,urine TGF-β1,PAI-1 and VEGF levels before treatment and at 3,6,12 months after treatment were compared between the two groups.The occurrence situation of adverse reactions was recorded.Results The 24 h urinary protein levels at 3,6,12 months after treatment in the two groups were decreased,moreover the 24 h urine protein level at each time point in the observation group was lower than that in the control group,the difference was statistically significant (P<0.05).The levels of Scr,BUN,urine TGF-β1,PAI-1 and VEGF after treatment in the two groups were decreased compared with before treatment,while the Alb level was increased compared with before treatment,moreover the levels of Scr,BUN,urine TGF-β1,PAI-1 and VEGF in the observation group were lower than those in the control group,while the Alb level was higher than that in the control group,the difference was statistically significant (P<0.05).The observation group appeared 2 cases of leukopenia,1 case of liver dysfunction and no serious adverse reactions occurred.Conclusion Tripterygium polyglycoside combined with cozaar has a significant therapeutic effect on elderly patients with IgAN,can significantly reduce urinary protein and protect renal function,moreover its clinical use is safer.Its efficacy may be related to reducing the expression levels of TGF-β1,PAI-1 and VEGF.

Objective To investigate the clinical efficacy of tripterygium wilfordii in the treatment of early diabetic nephropathy and its mechanism .Methods 86 patients with early diabetic nephropathy admitted to Jiaxing Hospital of Zhejiang Provincial Armed Police Corps from December 2015 to December 2017 were selected as research subjects.They were randomly divided into two groups according to the digital table ,with 43 cases in each group .The control group was treated by conventional internal medicine , while the observation group was added tripterygium glycosides on the basis of the control group .The clinical efficacy of the two groups and the changes of serum matrix metalloproteinase-9 (MMP-9) and plasminogen activator -1 (PAI-1) before and after treatment were compared . Results The total effective rate of the observation group was significantly higher than that of the control group (86.04％vs.58.14％)(χ2 =8.323,P=0.004).The MMP-9 and PAI-1 levels and urinary protein of the two groups after treatment were significantly improved ,but the changes of the observation group [ ( 57 .36 ±10 .24 ) ng/L, (24.39 ±7.66)ng/mL,(70.35 ±12.58)μg/min] were more significant than those of the control group [(85.62 ± 15.42)ng/L,(29.64 ±8.61)ng/mL,(102.57 ±20.36)μg/min](t=10.011,P<0.001;t=2.987,P=0.004;t=3.828,P<0.001).Conclusion The therapeutic effect of tripterygium wilfordii in the treatment of early diabetic nephropathy is significant .The mechanism is related to improving the expression of MMP -9 in kidney tissue and reducing the level of PAI-1.

Epigenetics,a branch of molecular biology,plays a pivotal role in the pathological progression of ischemic stroke.Epigenetic modifications are intricately involved in the complex and dynamic processes that regulate gene expression,cellular injury response,motor function,and cognitive ability following stroke.This provides an effective framework for elucidating the targets and mechanisms of action underlying traditional Chinese medicine's treatment of ischemic stroke.Currently,the etiology and pathogenesis of ischemic stroke remain incompletely understood,with modern medical treatments still lacking sufficient efficacy.Traditional Chinese medicine possesses a unique advantage in treating ischemic stroke through its multi-level and multi-target comprehensive regulation.Recent studies have discovered that traditional Chinese medicine can participate in regulating abnormal epigenetic modifications during stroke treatment.This article primarily focuses on the theoretical foundation of traditional Chinese medicine for strokes by exploring its application in DNA methylation,non-coding RNA,histone modification research as well as explaining the epigenetic effects it exerts when treating strokes.The aim is to provide insights for future research and development of traditional Chinese medicine for cerebral ischemia.

AIM:To explore the protective effect of Xiaoxuming decoction(XXMD)on synaptic plasticity in the context of cerebral ischemia-reperfusion injury following ischemic stroke.METHODS:An oxygen-glucose depriva-tion/reoxygenation(OGD/R)model was employed in vitro using mouse hippocampal neurons(HT22 cells)to simulate ischemia-reperfusion injury.Cell viability was assessed using a CCK-8 assay to determine the optimal XXMD concentra-tion.The HT22 cells were divided into two groups:control and model(OGD/R).Cellular morphological changes were ob-served using an inverted microscope.The levels of IL-1β,IL-6 and TNF-α in the supernatant were quantified by ELISA.Ultrastructural changes were examined by transmission electron microscopy.Immunofluorescence staining was used to de-tect neuron markers NeuN and synaptic proteins NF200 and MAP2.The protein levels of NF200 and MAP2 were analyzed by Western blot.RESULTS:The highest cell survival rate occurred at an XXMD concentration of 100 mg/L(P<0.05).Compared with control group,the cells in model group exhibited round shape and shrinkage,mitochondrial swelling or vacuolization,and a marked decrease in survival rate.There were significant increases in IL-1β,IL-6 and TNF-α levels(P<0.05).Immunofluorescence intensity and protein levels of NeuN,NF200 and MAP2 were notably reduced(P<0.05).Treatment with XXMD improved cell morphology,ultrastructure and survival rate(P<0.05),and decreased in-flammatory factor levels(P<0.05).Compared with model group,the cells in OGD/R+XXMD group showed significantly increased immunofluorescence intensity and protein levels of NeuN,NF200 and MAP2(P<0.05).CONCLUSION:Xiaoxuming decoction may mitigate OGD/R-induced injury,potentially by inhibiting inflammatory responses and enhanc-ing synaptic plasticity.

Objective: To analyze the delayed effect of candesartan ester combined with tripterygium wilfordii on renal failure of chronic kidney disease (CKD) from 2 to 3. Methods: From May 2015 to May 2016, 80 patients with chronic renal insufficiency (CRF) in Jiaxing Hospital of Zhejiang Provincial Armed Police Corps were selected in the research.The patients were randomly divided into the combined group and control group by compute random grouping method, with 40 cases in each group.The combined group was given candesartan ester combined with tripterygium wilfordii glycosides, and the control group was given glucocorticoid treatment.The therapeutic effect, the incidence of adverse reactions, improvement of clinical indicators and degree of kidney damage were compared between the two groups. Results: The total effective rate of the combined group was 95%, which was higher than 80% of the control group (χ²=4.116, P<0.05). The incidence of adverse reactions in the combined group was 7.5%, which was significantly lower than that in the control group (χ²=6.657, P<0.05). The biochemical parameters of the two groups had no statistically significant differences(t=1.032, 0.835, 1.017, 0.924, all P>0.05), but the serum urea nitrogen (BUN), serum creatinine (Scr), glomerular filtration rate (GFR) and uric acid levels in the combined group were (6.3±1.2)mmol/L, (99.6±4.5)μmol/L, (82.7±6.5)mL/min and (335.2±28.6)μmol/L, respectively, which were significantly better than those of the control group[(7.9±2.5)mmol/L, (128.9±6.4)moL/L, (59.6±7.3)mL/min and (437.9±37.1)mol/L](t=7.812, 8.119, 7.523, 8.981, all P<0.05). Before treatment, the renal damage degree between the two groups had no statistically significant difference (P>0.05). After treatment, the proportions of renal damage degree stage Ⅰ, Ⅱ, Ⅲ and Ⅳ in the combined group were 72.5%, 12.5%, 15.0% and 0.00%, respectively, which were significantly lower than those in the control group (22.5%, 32.5%, 37.5% and 7.5%) (χ²=20.058, 4.592, 5.237, 1.394, all P<0.05). Conclusion Candesartan ester combined with tripterygium wilfordii can be effectively used in the treatment of CKD at 2 to 3 stages, and the incidence of adverse reactions of drugs is relatively low, which can effectively improve the clinical indicators of patients and has a good retarding effect on renal failure.Therefore, it is recommended to be widely used in clinical treatment.

High mobility group box 1 (HMGB1) has been reported to play an important role in experimental autoimmune encephalomyelitis (EAE). Astrocytes are important components of neurovascular units and tightly appose the endothelial cells of microvessels by their perivascular endfeet and directly regulate the functions of the blood-brain barrier. Astrocytes express more HMGB1 during EAE while the exact roles of astrocytic HMGB1 in EAE have not been well elucidated. Here, using conditional-knockout mice, we found that astrocytic HMGB1 depletion decreased morbidity, delayed the onset time, and reduced the disease score and demyelination of EAE. Meanwhile, there were fewer immune cells, especially pathogenic T cells infiltration in the central nervous system of astrocytic HMGB1 conditional-knockout EAE mice, accompanied by up-regulated expression of the tight-junction protein Claudin5 and down-regulated expression of the cell adhesion molecules ICAM1 and VCAM1 in vivo. In vitro, HMGB1 released from astrocytes decreased Claudin5 while increased ICAM1 and VCAM1 expressed by brain microvascular endothelial cells (BMECs) through TLR4 or RAGE. Taken together, our results demonstrate that HMGB1 derived from astrocytes aggravates EAE by directly influencing the immune cell infiltration-associated functions of BMECs.
Mice ; Animals ; Encephalomyelitis, Autoimmune, Experimental/metabolism* ; Astrocytes/metabolism* ; HMGB1 Protein/metabolism* ; Endothelial Cells/metabolism* ; Mice, Inbred C57BL ; Mice, Knockout ; Blood-Brain Barrier/metabolism*