Urinary exosomal microRNA-145-5p and microRNA-27a-3p act as noninvasive diagnostic biomarkers for diabetic kidney disease

BACKGROUND Diabetic kidney disease(DKD),characterized by increased urinary microalbumin levels and decreased renal function,is the primary cause of end-stage renal di-sease.Its pathological mechanisms are complicated and multifactorial;Therefore,sensitive and specific biomarkers are needed.Urinary exosome originate from diverse renal cells in nephron segments and partially mirror the pathological changes in the kidney.The microRNAs(miRNAs)in urinary exosome are remark-ably stable and highly tissue-specific for the kidney.METHODS Type 2 diabetic mellitus(T2DM)patients were recruited from the Second Hospital of Hebei Medical University and were divided into two groups:DM,diabetic pa-tients without albuminuria[urinary albumin to creatinine ratio(UACR)<30 mg/g]and DKD,diabetic patients with albuminuria(UACR≥30 mg/g).Healthy subjects were the normal control(NC)group.Urinary exosomal miR-145-5p,miR-27a-3p,and miR-29c-3p,were detected using real-time quantitative polymerase chain reaction.The correlation between exosomal miRNAs and the clinical in-dexes was evaluated.The diagnostic values of exosomal miR-145-5p and miR-27a-3p in DKD were determined using receiver operating characteristic(ROC)analysis.Biological functions of miR-145-5p were investigated by performing RESULTS Urinary exosomal expression of miR-145-5p and miR-27a-3p was more upregulated in the DKD group than in the DM group(miR-145-5p:4.54±1.45 vs 1.95±0.93,P<0.001;miR-27a-3p:2.33±0.79 vs 1.71±0.76,P<0.05)and the NC group(miR-145-5p:4.54±1.45 vs 1.55±0.83,P<0.001;miR-27a-3p:2.33±0.79 vs 1.10±0.51,P<0.001).The exosomal miR-145-5p and miR-27a-3p positively correlated with albuminuria and serum creatinine and negatively correlated with the estimated glomerular filtration rate.miR-27a-3p was also closely related to blood glucose,gly-cosylated hemoglobin A1c,and low-density lipoprotein cholesterol.ROC analysis revealed that miR-145-5p had a better area under the curve of 0.88[95%confidence interval(CI):0.784-0.985,P<0.0001]in diagnosing DKD than miR-27a-3p with 0.71(95%CI:0.547-0.871,P=0.0239).Bioinformatics analysis revealed that the target genes of miR-145-5p were located in the actin filament,cytoskeleton,and extracellular exosome and were involved in the pathological processes of DKD,including apoptosis,inflammation,and fibrosis.CONCLUSION Urinary exosomal miR-145-5p and miR-27a-3p may serve as novel noninvasive diagnostic biomarkers or promising therapeutic targets for DKD.

Clinical Nursing Intervention of Moxibustion on Abdominal Distension Symptoms in Heart Failure (Heart and Kidney Yang Deficiency and Blood Stasis Blocking Collaterals Syndrome)

Objective:To investigate the clinical nursing intervention effect of moxibustion on abdominal distension symptoms in heart failure(heart and kidney yang deficiency and blood stasis blocking collaterals syndrome).Methods:62 patients with heart failure(heart and kidney yang deficiency and blood stasis blocking collaterals syndrome)admitted to our hospital from February 2023 to February 2024 were selected and divided into the observation group(n=31)and the control group(n=31)by using the random numerical table method.The control group adopted conventional nursing interventions,and the observation group received the nursing program of the control group with the addition of moxibustion nursing interventions.The nursing effectiveness,quality of life scores,and nursing satisfaction were compared between the two groups.Results:The nursing effectiveness of the observation group was significantly higher than the control group(P<0.05);the quality of life score of the observation group was significantly higher than the control group(P<0.05);the nursing satisfaction of the observation group was significantly higher than that of the control group(P<0.05).Conclusion:The use of moxibustion nursing intervention in patients with heart failure(heart and kidney yang deficiency and blood stasis blocking collaterals syndrome)can effectively relieve the symptoms of abdominal distension,improve patients'quality of life,and increase nursing satisfaction,which has promotion and application values.

Transcriptomic and metabolomic analysis of the effects of Zhenwu decoction on kidney yang deficiency pattern in chronic kidney disease

Objective:To explore the kidney yang deficiency pattern(KYDP)in a chronic kidney disease(CKD)rat model and the mechanisms underlying the effects of Zhenwu decoction(ZWD)by conducting tran-scriptomic and metabolomic analyses.Methods:Adriamycin(ADR)combined with hydrocortisone(HC)was used to induce CKD with KYDP in rats.ADR was injected into the tail vein twice.HC was injected intramuscularly for 8 weeks.ZWD was administered by gavage for 8 weeks.The general condition was observed,24-h urine protein was detected,serum corticosterone,triiodothyronine,thyroxine,TSH,testosterone,cAMP,and cGMP levels were determined,and pathological analysis was conducted.Transcriptomic and metabolomic analyses were conducted to screen differentially expressed genes(DEGs),differentially expressed metabolites(DEMs),and differentially expressed pathways(DEPs).The core DEMs and DEGs were input to Metab-oanalyst 5.0 to identify the pathways affected by ZWD.Results:In the HC group,KYDP symptoms were observed.Compared with control group,the levels of 24-h urine protein,TSH,and cGMP significantly increased(all P<0.01),and corticosterone,triiodothyronine,thyroxine,and cAMP significantly decreased(all P<0.01)in the HC group.After ZWD intervention,the levels of above-mentioned indicators could be reversed to some extent.Pathological analysis in the HC group revealed kidney lesions.DEGs in the ZWD group were mainly associated with pathways such as nucleotide synthesis and endocrine pathways.In the ZWD group,differences in biosynthesis of unsat-urated fatty acids and butanoate metabolism were observed.The following pathways were significantly affected by ZWD:arachidonic acid metabolism,valine,leucine,and isoleucine biosynthesis,linoleic acid metabolism,and alpha-linolenic acid metabolism.Conclusion:ZWD can be used to treat KYDP in CKD through regulating arachidonic acid metabolism,valine,leucine,and isoleucine biosynthesis,linoleic acid metabolism,and alpha-linolenic acid metabolism.

The Role for AVE0991 (MAS-Receptor Angiotensin II (1-7) Agonist) in Reducing Cisplatin-Induced Acute Kidney Injury on C57BL/6 Mice

Acute Kidney Injury (AKI) is a condition that causes nephrotoxicity in kidney tissues due to cisplatin-induced cancer treatments. Hence, it is proposed in this review that AVE0991 (a MAS-receptor Angiotensin II (1-7) agonist) may reduce cisplatin-induced acute kidney injury by promoting nitric oxide production.

Proteomics analysis of IBS-D with spleen and kidney yang deficiency

Objective:To investigate the molecular mechanism underlying the development of diarrhea-predominant irritable bowel syndrome (IBS-D) with spleen and kidney yang deficiency (SKYD) using a proteomics approach.Methods:Male Sprague-Dawley rats (n =22) were divided into IBS-D (n =12) and normal control (n =10) groups.SKYD was then modeled in IBS-D rats by a combination of acetic acid enema,bondage,rectal dilation,tail stimulation,and Senna gavage.Colon tissue samples were subsequently collected and examined by Q Exactive mass spectrometry to identify differentially expressed proteins between the two groups.Results:The occurrence of SKYD/IBS-D was associated with ribosomal protein S23 (Rps23),protein phosphatase 2 catalytic subunit alpha (Pp2a),and growth factor receptor-bound protein 2 (Grb2),which are involved in the ribosome,neurotrophin signaling,and Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathways.Conclusion:These data suggest that SKYD/IBS-D pathophysiology likely involves inflammation,cell growth,apoptosis,stress granule formation,immune activation,loss of epithelial cell integrity,and visceral hypersensitivity.

Biological function of miRNA-145-5p in angiotensin II induced renal inflammation

Objective:Chronic kidney disease(CKD)is a progressive disorder characterized by intricate structural and functional alterations in the kidneys,attributable to diverse causative factors.Notably,the therapeutic promise of miR-145-5p in addressing renal pathologies has been discerned.This investigation seeks to elucidate the functional role of miR-145-5p in injured kidneys by subjecting human glomerular mesangial cells(HGMCs)to stimulation with Angiotensin II(AngII).Materials and Methods:Cellular viability and the levels of inflammatory mediators were evaluated utilizing Cell Counting Kit-8(CCK-8),quantitative real-time polymerase chain reaction(qRT-PCR),and western blot methodologies,both in the presence of AngII incubation and in scenarios of miR-145p overexpression and downregulation.Furthermore,the cell cycle dynamics were elucidated through Fluorescence-activated Cell Sorting(FACS)analysis.Results:AngII incubation induced an upregulation of miR-145-5p and inflammatory factors including Intercellular Adhesion Molecule 1(ICAM-1),Interleukin 6(IL-6),Interleukin 8(IL-8),and Interleukin 1β(IL-1β).Additionally,it elevated the expression of Cyclin A2,Cyclin D1,and the G2/M cell cycle ratio.Conversely,inhibition of miR-145-5p heightened the levels of inflammatory factors and cell cycle regulators induced by AngII incubation.Reduced expression of miR-145-5p correlated with a downregulation of Interleukin 10(IL-10)expression,concurrently promoting HGMC proliferation under AngII stimulation.Moreover,ectopic miR-145-5p expression demonstrated a reduction in inflammatory factors,cell cyclin regulators,G2/M cell cycle ratio,and overall proliferation.Conclusion:MiR-145-5p exhibited inhibitory effects on the inflammatory response and proliferation induced by Angiotensin II in HGMCs,showcasing its potential as a therapeutic avenue for the treatment of kidney injury.

Clinical observation on efficacy of compound of warming yang, descending turbidity and dredging collaterals in the treatment of diabetic kidney disease with Yin-Yang deficiency and blood stasis syndrome

Objective:To observe the clinical efficacy of compound of owarming yang,descending turbidity and dredging collaterals in the treatment of diabetic kidney disease with yin-yang deficiency and blood stasis syndrome.Methods:Seventy-six patients of diabetic kidney disease with yin-yang deficiency and blood stasis syndrome were randomly divided into observation group and control group,thirty-eight cases in each group.The control group was given conventional western medicine treatment,while the observation group took compound of owarming yang,descending turbidity and dredging collaterals orally on the basis of conventional western medicine treatment.The course of treatment covered for one month.Before and after treatment,we observed the scores of traditional Chinese medicine symptoms,indicators of renal function[serum creatinine(Scr),blood urea nitrogen(BUN),microalbuminuria(MALB)],indicators of glucose metabolism[fasting plasma glucose(FPG),2-hour postprandial blood glucose(2hPG),glycosylated hemoglobin(HbAlc)],indicators of hemorheology[plasma viscosity(PV),platelet aggregation rate(PAR),fibrinogen(FIB)],Cystatin-C(Cys-C),C-reactive protein(CRP)in the two groups.Results:After treatment,the clinical effect of the observation group was significantly better than the control group(P<0.05).The scores of traditional Chinese medicine symptoms,indicators of renal function(Scr、BUN、UAER),indicators of glucose metabolism(FPG、2hPG、HbAlc),indicators of hemorheology(PV、PAR、FIB),Cys-C and CRP in the two groups were decreased significantly compared with those before treatment(P<0.05),and the decrease in the observation group was superior to that in the control group(P<0.05).Conclusion:Compound of warming yang,descending turbidity and dredging collaterals has remarkable efficacy in treating of diabetic kidney disease patients with yin-yang deficiency and blood stasis syndrome by alleviating clinical symptoms,glucose metabolism,renal function and microcirculatory disturbance,and the mechanism related to alleviation of microinflammation.

Metformin regulates inflammation and fibrosis in diabetic kidney disease through TNC/TLR4/NF-κB/miR-155-5p inflammatory loop

BACKGROUND Type 2 diabetes mellitus(T2DM)is significantly increasing worldwide,and the incidence of its complications is also on the rise.One of the main complications of T2DM is diabetic kidney disease(DKD).The glomerular filtration rate(GFR)and urinary albumin creatinine ratio(UACR)increase in the early stage.As the disease progresses,UACR continue to rise and GFR begins to decline until endstage renal disease appears.At the same time,DKD will also increase the incidence and mortality of cardiovascular and cerebrovascular diseases.At present,the pathogenesis of DKD is not very clear.Therefore,exploration of the pathogenesis of DKD to find a treatment approach,so as to delay the development of DKD,is essential to improve the prognosis of DKD.AIM To detect the expression of tenascin-C(TNC)in the serum of T2DM patients,observe the content of TNC in the glomerulus of DKD rats,and detect the expression of TNC on inflammatory and fibrotic factors in rat mesangial cells(RMCs)cultured under high glucose condition,in order to explore the specific molecular mechanism of TNC in DKD and bring a new direction for the treatment of DKD.METHODS The expression level of TNC in the serum of diabetic patients was detected by enzyme-linked immunosorbent assay(ELISA),the protein expression level of TNC in the glomerular area of DKD rats was detected by immunohistochemistry,and the expression level of TNC in the rat serum was detected by ELISA.Rat glomerular mesangial cells were cultured.Following high glucose stimulation,the expression levels of related proteins and mRNA were detected by Western blot and polymerase chain reaction,respectively.RESULTS ELISA results revealed an increase in the serum TNC level in patients with T2DM.Increasing UACR and hypertension significantly increased the expression of TNC(P<0.05).TNC expression was positively correlated with glycosylated haemoglobin(HbA1c)level,body mass index,systolic blood pressure,and UACR(P<0.05).Immunohistochemical staining showed that TNC expression in the glomeruli of rats with streptozotocin-induced diabetes was significantly increased compared with normal controls(P<0.05).Compared with normal rats,serum level of TNC in diabetic rats was significantly increased(P<0.05),which was positively correlated with urea nitrogen and urinary creatinine(P<0.05).The levels of TNC,Toll-like receptor-4(TLR4),phosphorylated nuclear factor-κB p65 protein(Ser536)(p-NF-κB p65),and miR-155-5p were increased in RMCs treated with high glucose(P<0.05).The level of TNC protein peaked 24 h after high glucose stimulation(P<0.05).After TNC knockdown,the levels of TLR4,p-NF-κB p65,miR-155-5p,connective tissue growth factor(CTGF),and fibronectin(FN)were decreased,revealing that TNC regulated miR-155-5p expression through the TLR4/NF-κB p65 pathway,thereby regulating inflammation(NF-κB p65)and fibrosis(CTGF and FN)in individuals with DKD.In addition,metformin treatment may relive the processes of inflammation and fibrosis in individuals with DKD by reducing the levels of the TNC,p-NF-κB p65,CTGF,and FN proteins.CONCLUSION TNC can promote the occurrence and development of DKD.Interfering with the TNC/TLR4/NF-κB p65/miR-155-5p pathway may become a new target for DKD treatment.

环孢素引起肾小管上皮细胞培养液中肾损伤分子-1水平升高的机制

目的:探讨环孢素(CsA)引起人肾小管上皮细胞(HKC)培养液中肾损伤分子-1(KIM-1)水平升高的作用机制,阐明KIM-1表达与p38 MAPK通路和EKR1/2 MAPK通路的关系。方法:将处于对数生长期的HKC分为空白组、CsA损伤组、CsA与p38激酶抑制剂合用组、p38激酶抑制剂组、CsA与ERK1/2激酶抑制剂合用组和ERK1/2激酶抑制剂组。MTT法检测各组HKC增殖抑制率,ELISA法测定各组HKC上清液中KIM-1水平,流式细胞术检测各组细胞存活率、细胞凋亡率和细胞坏死率。结果:与空白组比较,CsA损伤组细胞上清液中KIM-1水平显著升高(P<0.05),细胞存活率显著降低(P<0.05),细胞凋亡率和细胞坏死率显著升高(P<0.05);p38激酶抑制剂组和ERK1/2激酶抑制剂组中细胞存活率、细胞凋亡率和细胞坏死率比较差异无统计学意义(P>0.05)。与CsA损伤组比较,CsA与p38激酶抑制剂合用组、CsA与ERK1/2激酶抑制剂合用组细胞上清液中KIM-1水平显著降低(P<0.05),细胞存活率显著升高(P<0.05),细胞凋亡率和细胞坏死率显著降低(P<0.05)。结论:p38 MAPK通路和ERK1/2 MAPK通路参与CsA素引起肾小管上皮细胞培养液中KIM-1水平升高的过程,KIM-1的表达可能成为临床监测CsA肾毒性的生化指标。

体外循环心脏不停跳二尖瓣置换术围术期肾损伤分子-1的变化

目的研究体外循环(CPB)心脏不停跳与停跳二尖瓣置换术(MVR)围术期尿肾损伤分子-1(KIM-1)的变化规律,探讨心脏不停跳手术对患者肾功能的影响。方法选择需行MVR患者40例,按随机数字表分为不停跳组和停跳组,每组各20例。检测术前(T1)、CPB后30 min(T2)、2 h(T3)、术后24 h(T4)、72 h(T5)的KIM-1浓度。结果组内不同时间点的KIM-1浓度差异有统计学意义(P<0.05),随着时间延长两组KIM-1浓度上升,但不停跳组术后72 h恢复至正常水平,而停跳组72 h后仍未能恢复至术前水平。不停跳组KIM-1浓度低于停跳组(P<0.05)。结论 CPB心脏不停跳MVR患者围术期尿KIM-1浓度变化较小,心脏不停跳手术或可减少肾功能损害。

Art of Nourishing Life According to the Kidney Meridian in Zhenjiu Dacheng(The Great Compendium of Acupuncture and Moxibustion)

“Daoyin Benjing”(Art of Nourishing Life)discusses the kidney meridian in depth.It is a dense and heterogeneous text that is heavily influenced by Daoism.The text proposes rules for the maintenance of life using language that is often cryptic and under-standable only to the initiated.This language is closely interwoven with the classical terms of traditional Chinese medicine.The kidney is the home of vital energy,which is a type of sexual energy and the root of life.Engagement in moderate sexual activity nourishes life and leads to a long life.This is the goal of every Daoist follower and the goal of every doctor.

Microalbuminuria in hepatitis C-genotype 4:Effect of pegylated interferon and ribavirin

AIM:To study the relation between hepatitis C virus (HCV) genotype 4 and microalbuminuria and renal impairment in relation to hepatic histology, and viremia in the absence of cryoglobulinemia, and to examine the effect of treatment on microalbuminuria.METHODS: Three hundred subjects, including 233 HCV genotype-4 infected patients, were tested for cryoglobulinemia, microalbuminuria, albumin creatinine ratio (ACR), urea, creatinine, and estimated glomerular filtration rate (eGFR). The parameters were measured again in the HCV patients after 48 wk of treatment with pegylated interferon and ribavirin.RESULTS: Significantly higher levels of microalbumin- uria were detected in HCV-positive patients compared to HCV-negative controls (median 9.5 vs 5.9, respectively, Kruskal-Wallis P=0.017). Log microalbuminuria was significantly correlated with hepatic inflammation (r=0.13, P=0.036) and f ibrosis (r=0.12, P=0.061), but not with viral load (r=-0.03, P=0.610), or alanine transaminase (r=-0.03, P=0.617). Diabetes mellitus neither significantly moderated (χ2=0.13, P=0.720), nor mediated (Sobel test P=0.49) the HCV effect. HCV status was signifi cantly associated with log microalbu-minuria (χ2=4.97, P=0.026), adjusting for age, gender, diabetes, cryoglobulinemia, urea and creatinine. A positive HCV status was not significantly associated with low eGFR (<60 mL/min every 1.73 m2) [odds ratio (OR): 0.5, 95% confidence interval (CI):0.2-1.4], nor with high ACR (OR: 1.7, 95% CI:0.7-4.1). End-of-treatment response (ETR) was achieved in 51.9% of patients. Individuals with ETR had significantly lower microalbuminuria post-treatment (χ2=8.19, P=0.004).CONCLUSION: HCV affected the development of microalbuminuria independent of diabetes or cryoglobulinemia. Combination therapy of pegylated interferon-ribavirin had a positive effect in reducing microalbuminuria.

Losartan Protects Podocytes against High Glucose-induced Injury by Inhibiting B7-1 Expression

The role of B7-1 in podocyte injury has received increasing attention.The aim of this study was to investigate whether losartan protects podocytes of patients with diabetic kidney disease(DKD)by regulating B7-1 and the underlying mechanisms.Rats with streptozotocin-induced DKD were treated with losartan for 8 weeks.Biochemical changes in blood and urine were analyzed.Kidneys were isolated for electron microscopy,immunofluorescence,real-time quantitative PCR(RT-PCR),and Western blot analysis.Immortalized mouse podocyte cells were cultured in normal or high glucose medium in the presence or absence of losartan for 48 h,and then the cells were collected for immunofluorescence,PCR,Western blotting and monolayer permeability detection.The phosphatidylinositol 3-kinase(PI3K)110a subunit and angiotensin II type 1 receptor(AT1R)plasmids were transfected into podocytes,respectively,and then Western blotting was performed to assess the expression of B7-1 protein.The results showed that losartan ameliorated podocyte structure and function in the rat model of DKD,and reduced the expression of B7-1 protein.Overexpression of PI3K 110a subunit in podocytes attenuated the inhibitory effect of losartan on B7-1 expression in high glucose-stimulated podocytes.The expression of B7-1 was significantly increased by overexpression of ATI R and significantly reduced by blocking PI3K 110a subunit.We conclude that losartan protects podocytes against high glucose-induced injury by inhibiting AT1R-mediated B7-1 expression.This effect is dependent on the AT1R-PI3K 110a subunit pathway.

Question of Parity Non-conservation in Weak Interactions

In order to reasonably explain the phenomenon of cell bioelectricity,we proposed the conservation law of cell membrane area,established the ion inequality equation,and therefore paid attention to the mystery of“θ-τ”.We researched and analyzed the“θ-τ”mystery,discussed the parity non-conservation in weak interactions,suggested possible experiments to test the parity non-conservation in weak interactions,and gave our research and analysis conclusions:The parity non-conservation in weak interactions,is still a“conjecture”;The experimental scheme suggested in the papers by C.N.Yang et al.cannot determine whether the weak interaction can separate left and right,and it is impossible to directly answer whetherθandτin the“θ-τ”mystery are the same particle;The Co60βdecay experiment such as C.S.Wu is a pseudo-mirror experiment,whether the experimental result violates parity conservation is only based on the assumption of C.N.Yang et al.In fact,experiments such as polarized Co60 did not overturn the so-called“law of parity conservation”.The mirror image principle does not have any physical meaning,does not correspond to any physical conservation quantity,and cannot be destroyed by any physical experiment.In the process of turning“mirror symmetry”and“mirror asymmetry”into so-called physical“common sense”and scientific“facts”respectively,the methods of transformation are“stealing concepts”and“circular argumentation”.The“θ-τ”mystery is a“man-made”mystery.θandτare two different particles,which may be the result of the same precursor particle being divided into two.The work of C.N.Yang,T.D.Lee,C.S.Wu et al.has brought quantum physicists from the“small black room”to the“bigger black room”or“smaller black room”.The right and wise choice is to go back through the door that came in.With the development of science today,it is time for some contents to reform from the bottom.

Regulatory mechanism of hormones of the pituitary-target gland axes in kidney-Yang deficiency based on a support vector machine model

OBJECTIVE:To study the development mechanism of kidney-Yang deficiency through the establishment of support vector machine models of relevant hormones of the pituitary-target gland axes in rats with kidney-Yang deficiency syndrome.METHODS:The kidney-Yang deficiency rat model was created by intramuscular injection of hydrocortisone,and contents of the hormones of the pituita- ry-thyroid axis:thyroid stimulating hormone(TSH),3,3',5-triiodothyronine(T_3) and thyroxine(T_4);hormones of the pituitary-adrenal gland axis:adrenocorticotropic hormone(ACTH) and Cortisol(CORT);and hormones of the pituitary-gonadal axis:luteinizing hormone(LH),follicle-stimulating hormone(FSH),and testosterone(T),were determined in the early,middle,and advanced stages.Ten support vector regression(SVR) models of the hormones were established to analyze the mutual relationships among the hormones of the three axes.RESULTS:The feedback control action of the pituitary-adrenal axis began to lose efficacy from the middle stage of kidney-Kong deficiency.The contents all hormones of the three pituitary-target gland axes decreased in the advanced stage.Relative errors of the jackknife test of the SVR models all were less than 10%.CONCLUSION:Imbalances in mutual regulation among the hormones of the pituitary-target gland axes,especially loss of effectiveness of the pituitary-adrenal axis,is one pathogenesis of kidney-Yang deficiency.The SVR model can accurately reflect the complicated non-linear relationships among pituitary-target gland axes in rats with of kidney-Yang deficiency.

The Effect of Hormones of the Hypothalamic-pituitary-target Gland Axes in a Kidney-Yang Deficiency Syndrome Model

Kidney-yang deficiency syndrome(KYDS)is a diagnostic pattern in the traditional Chinese medicine.Studies have shown that KYDS is related to the functional disorder of hormones of the hypothalamic-pituitary-target gland axes.The standard procedure used to mimic KYDS is the injection of a high dose of exogenous glucocorticoid(hydrocortisone and corticosterone).Such a model showed symptoms such as exhaustion,body twists,cold limbs,lying crowded together,decreased rectal temperature,sexual dysfunction,decreased reaction speed,reduced spontaneous activity,hair loss,loss of appetite,and weight loss.Moreover,the model manifested an imbalance in mutual control among the hormones of the pituitary-target gland axes,including adrenocorticotrophic hormone,CORT,CRH,thyroid-stimulating hormone,triiodothyronine,thyroxine,T,E2,follicle-stimulating hormone,luteinizing hormone,and 17-OHCS.

Effect of Zhuchun Pill on Immunity and Endocrine Function of Senile Kidney-Yang Daficiency

Objective: To evaluate the effect of Zhuchun pill (ZCP) on senile Kidney-Yang Deficiency (KYD). Methods: By single blind method, 45 elderly males with KYD were divided randomly into the ZCP group (treated by ZCP) and the control group (treated by placebo, starch capsule) and treated for 3 months.Results: ZCP could greatly improve the main symptoms of KYD, P < 0. 01 in comparison with the control group. After treatment, in the ZCP group, the 3H-TdR lymphocyte transformation rate, levels of serum C3,IgA, IgD, IgG and IgM, superoxide dismutase, plasma adrenocortical hormone, testosterone and cyclic adenosine monophosphate all increased, P < 0. 01, and plasma lipid peroxide decreased, P < 0. 01. While in the control group, no remarkable change was found in these parameters. Conclusion: ZCP could improve the KYD through regulating the immunity, endocrine function and scavenging the free radicals in organism.

SnO_2微晶掺杂SiO_2玻璃薄膜的制备及光谱性质的研究

采用溶胶 -凝胶法成功地制备出SnO2 微晶掺杂SiO2 玻璃薄膜。通过X射线粉末衍射和晶胞常数计算确认了SnO2 纳米微晶均匀分布于玻璃基质中 ;由薄膜的室温透射光谱研究发现 ,随热处理温度的升高、热处理时间的延长 ,薄膜的透射光谱向长波方向移动 ,表现出明显的量子尺寸效应。

长蛇灸对肾阳虚大鼠HPA轴及肝脏11β-HSD1的影响

Objective:To observe the effects of long-snake moxibustion on the hypothalamic-pituitary-adrenocortical(HPA)axis and hepatic 11β-hydroxy steroid dehydrogenase type 1(11β-HSD1)expression in rats with kidney yang deficiency to provide a basis for later in-depth exploration of the action mechanism of longsnakemoxibustion on suchrats.Methods:Fifteen SPF-grade,male,SD rats were randomly divided into a blank control group,a model group,and a long-snake moxibustion treatment group,with five rats in each group.Hydrocortisone powder(30 mg/kg)was administered by gavage at a volume of 10 mL/kg to prepare the rat model of kidney yang deficiency.After successful modeling,the rats in the long-snake moxibustion treatment group underwent long-snake moxibustion treatment every other day along the governor vessel from Dazhui(GV14)to Shenshu(BL23),for a period of 14 days.The remaining two groups were secured in the same way as the long-snake moxibustion treatment group,although they did not receive any treatment.The body weight,rectal temperature,and spontaneous activity count of the rats,as well as serum levels of corticotropin releasing hormone(CRH)and corticosterone(CORT)were detected by ELISA before modeling,after modeling,and after treatment.The amount of 11β-HSD1 protein in rat liver was determined by immunohistochemistry and Western blot analysis.Results:Compared with the rats in the blank control group,those in the model group exhibited a significant decrease in the trend of body weight growth and in rectal temperature(P<0.05),as well as a slight yet non-significant decrease in spontaneous activity count(P>0.05);compared with the rats in the model group,the rats in the treatment group exhibited a significant increase in rectal temperature(P<0.05)and in spontaneous activity count(P<0.05).Moreover,after 14 days of treatment,compared with the rats in the blank,the rats in the model group exhibited a significant decrease in serum cORT content(P<0.05)and in the expression of 11β-HSD1 in the liver(P<0.05),as well as a slight yet non-significant decrease in serum CRH content(P>0.05);compared with the rats in the model group,the rats in the treatment group exhibited a significant increase in serum CRH content(P<0.05)and in the expression of 11β-HSD1 in the liver(P<0.05),as well as a slight yet non-significant increase in serum CORT content(P>0.05).Conclusion:Long-snake moxibustion can increase the rectal temperature and spontaneous activity count of rats with kidney yang deficiency,improve the function of the HPA axis,and increase the expression of 11β-HSD1 in the liver.

Mechanism underlying treatment of diabetic kidney disease using Traditional Chinese Medicine based on theory of Yin and Yang balance

The pathogenic mechanism of diabetic kidney disease(DKD) is complex. The development of DKD cannot be fully explained by a single mechanism.Traditional Chinese Medicine(TCM) has been applied extensively for the treatment of DKD in China.However, studying the mechanism of DKD using theories and methods that are appropriate for TCM characteristics and searching for theoretical bases for TCM clinical application are topics that still need to be explored and researched. Activation of the transforming growth factor(TGF)-β1/Smad and PI3 K/Akt/mTOR signaling pathways functions as a self-protection mechanism against renal microinflammation in DKD. However, the persistent abnormal overactivation of reactions causes secondary cell dysfunction, cell apoptosis, increased extracellular matrix(ECM) secretion, and eventually renal fibrosis. During this process, the dysregulation of self-balance among a variety of signaling pathways and the loss of self-feedback regulatory mecha-nisms downstream of these signaling pathways are critical causes of the occurrence and development of DKD. TCM may both inhibit the expression or activation of "hyperactive" signaling pathways(NFB, Smad3, and PI3 K/Akt/mTOR) and increase the expression or activation of "deficient" signaling pathways(Smad7 and PTEN) to restore balance to cells with an abnormal pathophysiological status and achieve the goal of DKD treatment.