RESUMO
On a global basis, potato cyst nematodes (Globodera spp. Skarbilovich 1959 [Behrens 1975]) are one of the most serious soilborne pathogens in potato (Solanum tuberosum L.) production. In 2019 to 2020, 188 soil samples were taken from rhizosphere soil associated with the roots of stunted and chlorotic potato plants in the main potato-growing areas of Yunnan and Sichuan Provinces of China. Globodera rostochiensis Wollenweber 1923 (Skarbilovich 1959) was recovered from 112 of the samples. Nematode identification was as confirmed by morphometric, light microscopy, electron microscopy, and molecular methodologies. Population densities of G. rostochiensis ranged from 47.0 to 69.0 eggs/g of soil. A BLASTn homology search program was used to compare the sequences of populations of G. rostrochienses from Yunnan and Sichuan Provinces with populations of other Heteroderinae spp. and populations of G. rostochiensis from other nations. Although potato has been grown in China for at least 400 years and the nation produces more potato than any other country, potato cyst nematodes were not reported in China until 2022.
Assuntos
Nematoides , Solanum tuberosum , Animais , China , SoloRESUMO
Glioma is the most commonly occurring primary neuroepithelial neoplasm. Long noncoding RNAs (lncRNAs) are emerging as pivotal modulators of gene expression in the immune system and play critical roles in the growth, progression, and immune response of carcinomas. In this study, we performed univariate Cox regression analysis on survival data from TCGA and identified 20 prognostic lncRNAs. Moreover, we revealed that these prognosis-related lncRNAs (PRLnc) were dysregulated in glioma. Furthermore, we constructed a signature based on the expression levels of these prognosis-related lncRNAs based on 13 prognostic lncRNAs, including AGAP2-AS1, CYTOR, MIR155HG, LINC00634, HOTAIRM1, SNHG18, LINC01841, LINC01842, LINC01426, MIR9-3HG, TMEM220-AS1, LINC00641, LINC01270, and LINC01503. The Kaplan-Meier curves show that high-risk patients had a shorter survival time. Finally, the glioma samples were classified into 2 subgroups based on the median expression of prognosis-related lncRNAs in each sample. In summary, these findings suggest that PRLnc is associated with tumor-infiltrating immune cells in glioma and that subtype 2 patients may respond more positively to immunotherapy.
RESUMO
Transforming growth factor (TGF)-ß/Smad signalling plays a central role in the pathogenesis of peritoneal fibrosis related to peritoneal dialysis (PD). Parthenolide (PTL), a naturally occurring phytochemical, is isolated from the shoots of feverfew (Tanacetum parthenium) and displays analgesia, anti-inflammation and anticancer activities. In this study, we examined the therapeutic potential of PTL on PD-related peritoneal fibrosis induced by daily intraperitoneal injection of 4.25% dextrose-containing PD fluid (PDF) in vivo and TGF-ß1-induced epithelial-mesenchymal transition (EMT) in vitro. PTL was administered daily before PDF injection or after 14â¯days of PDF injection. Both PTL treatments showed a protective effect on peritoneal fibrosis and prevented peritoneal dysfunction. Similarly, PTL suppressed the expression of fibrotic markers (fibronectin and collagen I) and restored the expression of the epithelial marker (E-cadherin) in TGF-ß1-treated HMrSV5 cells. Furthermore, PTL inhibited TGF-ß1-induced Smad2 and Smad3 phosphorylation and nuclear translocation but did not influence Smad1/5/9 phosphorylation or activate other downstream signalling pathways of TGF-ß1, including AKT, extracellular signal-regulated kinase (ERK) or p38. In conclusion, PTL treatment may represent an effective and novel therapy for PD-associated peritoneal fibrosis by suppressing the TGF-ß/Smad pathway.
Assuntos
Anti-Inflamatórios não Esteroides/farmacologia , Diálise Peritoneal/efeitos adversos , Fibrose Peritoneal/tratamento farmacológico , Sesquiterpenos/farmacologia , Transdução de Sinais/efeitos dos fármacos , Animais , Anti-Inflamatórios não Esteroides/uso terapêutico , Linhagem Celular , Soluções para Diálise/administração & dosagem , Soluções para Diálise/efeitos adversos , Modelos Animais de Doenças , Avaliação Pré-Clínica de Medicamentos , Transição Epitelial-Mesenquimal/efeitos dos fármacos , Transição Epitelial-Mesenquimal/imunologia , Feminino , Humanos , Masculino , Camundongos , Fibrose Peritoneal/etiologia , Fibrose Peritoneal/imunologia , Fibrose Peritoneal/patologia , Peritônio/citologia , Peritônio/efeitos dos fármacos , Peritônio/imunologia , Peritônio/patologia , Fosforilação/efeitos dos fármacos , Fosforilação/imunologia , Sesquiterpenos/uso terapêutico , Transdução de Sinais/imunologia , Proteínas Smad/imunologia , Proteínas Smad/metabolismo , Fator de Crescimento Transformador beta1/imunologia , Fator de Crescimento Transformador beta1/metabolismoRESUMO
Diabetic kidney disease (DKD) is the principal cause of end-stage renal disease worldwide and few treatments are available. Because immunomodulators are pivotal to DKD pathophysiology, anti-inflammatory agents may be useful for treating DKD. This study was conducted to investigate the effect of micheliolide (MCL), a novel guaianolide sesquiterpene lactone with well-known anti-inflammatory effects, on DKD. Treatment with dimethylaminomicheliolide (DMAMCL), the pro-drug of MCL currently under clinical trial in oncology, protected the kidneys against proteinuria, renal failure, histopathological injury, and inflammation in db/db mice. This effect was associated with metadherin (Mtdh) downregulation. We observed aberrant upregulation of Mtdh in the kidneys of db/db mice and high-glucose (HG)-induced mouse tubular epithelial cells (mTECs). Downregulation of Mtdh obviously inhibited nuclear factor-κB signaling activation and suppressed its downstream inflammatory cytokines, such as monocyte chemotactic peptide-1, interleukin-1ß, tumor necrosis factor-α, and interleukin-6 in HG-induced mTECs, which was similar to the effect of MCL. Mtdh overexpression largely reversed the anti-inflammatory role of MCL. Moreover, MCL downregulated Mtdh by both inhibiting the transcription level and promoting ubiquitin-mediated degradation. These findings suggest that DMAMCL is a promising anti-inflammatory agent useful for preventing renal injury in DKD by inhibiting Mtdh-mediated renal inflammation.
Assuntos
Anti-Inflamatórios/uso terapêutico , Diabetes Mellitus Experimental/tratamento farmacológico , Nefropatias Diabéticas/tratamento farmacológico , Pró-Fármacos/uso terapêutico , Sesquiterpenos de Guaiano/uso terapêutico , Animais , Anti-Inflamatórios/farmacologia , Células Cultivadas , Citocinas/genética , Citocinas/metabolismo , Diabetes Mellitus Experimental/genética , Diabetes Mellitus Experimental/metabolismo , Diabetes Mellitus Experimental/patologia , Nefropatias Diabéticas/genética , Nefropatias Diabéticas/metabolismo , Nefropatias Diabéticas/patologia , Regulação para Baixo , Células Epiteliais/efeitos dos fármacos , Rim/efeitos dos fármacos , Rim/metabolismo , Rim/patologia , Proteínas de Membrana/genética , Proteínas de Membrana/metabolismo , Camundongos , NF-kappa B/metabolismo , Pró-Fármacos/farmacologia , Proteínas de Ligação a RNA/genética , Proteínas de Ligação a RNA/metabolismo , Sesquiterpenos de Guaiano/farmacologiaRESUMO
Peritoneal fibrosis (PF) is a major cause of ultrafiltration failure in patients receiving long-term peritoneal dialysis (PD), and effective prevention and treatment strategies are urgently needed. The dimethylamino Michael adduct of a natural product-derived micheliolide (MCL), dimethylaminomicheliolide (DMAMCL), is a new lead compound with the advantages of high stability, low toxicity, and sustainable release of MCL. This study aimed to investigate the protective effect of DMAMCL against PD-related PF and the mechanisms involved. In this study, we found that DMAMCL significantly decreased PD-induced extracellular matrix (ECM) deposition in a mouse model of PD, and that delayed DMAMCL administration halted the progression of PF in an established PD model. In addition, rapamycin administration induced autophagy and significantly ameliorated PF. The protective effect of DMAMCL against PF was weakened when co-administered with DMAMCL and 3-methyladenine. Inducing autophagy by rapamycin decreased transforming growth factor-ß1-induced ECM accumulation in vitro. MCL promoted autophagy and inhibited ECM deposition. The anti-fibrotic effect of MCL was eliminated when knocking down ATG7 by siRNA. Taken together, DMAMCL might prevent against PF through activating autophagy. The anti-fibrotic effect of DMAMCL may be a new candidate for the treatment in patients with PD-related PF. KEY MESSAGES: Dimethylaminomicheliolide, the pro-drug of micheliolide, protects against peritoneal fibrosis in a mouse peritoneal dialysis model. Micheliolide inhibits TGF-ß1-induced extracellular matrix accumulation in vitro. Autophagy plays a protective role against peritoneal fibrosis. The antifibrogenic effect of dimethylaminomicheliolide may be due to the activation of autophagy.
Assuntos
Autofagia/efeitos dos fármacos , Fibrose Peritoneal/tratamento farmacológico , Substâncias Protetoras/uso terapêutico , Sesquiterpenos de Guaiano/uso terapêutico , Animais , Feminino , Masculino , Camundongos Endogâmicos C57BL , Diálise Peritoneal/efeitos adversos , Fibrose Peritoneal/etiologia , Fibrose Peritoneal/metabolismo , Fibrose Peritoneal/prevenção & controle , Substâncias Protetoras/farmacologia , Sesquiterpenos de Guaiano/farmacologia , Fator de Crescimento Transformador beta1/metabolismoRESUMO
AIM: Membranous nephropathy and minimal change disease (MCD) have been involved in mercury-induced nephrotic syndrome. IgA nephropathy is not known to be a common pathological type. In the present article, we report a case of IgA nephropathy with MCD following exposure to mercury-containing skin lightening cream. MATERIAL AND METHODS: The patient was a 39-year-old woman who presented with nephrotic syndrome. She had a 6-month history of using as many as 8 kinds of skin-lightening creams, and urinary mercury excretion was high. Renal biopsy revealed IgA nephropathy with MCD. The use of cosmetics was stopped and chelation therapy was given. After 4 courses (1 month) of chelation therapy, there was a complete remission of proteinuria and hematuria, and urine tests remained normal during the 5-year follow-up period. RESULTS AND CONCLUSIONS: The unique clinical and pathological features of IgA nephropathy with MCD had raised the controversial question of whether MCD and IgA deposition are separate entities or a common pathophysiology. Repeated renal biopsy and similar cases were helpful and should be carried out as far as possible.â©.
Assuntos
Glomerulonefrite por IGA/induzido quimicamente , Intoxicação por Mercúrio/complicações , Nefrose Lipoide/induzido quimicamente , Preparações Clareadoras de Pele/intoxicação , Adulto , Quelantes/uso terapêutico , Feminino , Glomerulonefrite por IGA/patologia , Glomerulonefrite por IGA/terapia , Hematúria/etiologia , Humanos , Rim/patologia , Rim/ultraestrutura , Intoxicação por Mercúrio/tratamento farmacológico , Nefrose Lipoide/patologia , Nefrose Lipoide/terapia , Síndrome Nefrótica/etiologia , Síndrome Nefrótica/terapia , Proteinúria/etiologia , Indução de Remissão , Preparações Clareadoras de Pele/química , Unitiol/uso terapêuticoRESUMO
OBJECTIVE: To investigate the effect of the serum of rats fed with Shenkang pill in regulating monocyte chemoattractant protein 1 (MCP-1) expression induced by advanced oxidation protein products (AOPP) in mouse podocyte clone 5 (MPC5) and explore the underlying mechanism. METHODS: MPC5 cultured in vitro were incubated for different time lengths in the presence of different concentrations of serum of rats medicated with Shenkang pill, and the cell proliferation was assessed using MTT assay. In MPC5 treated with AOPP prior to exposure to the rat serum, the changes in the protein expressions of p38MAPK and IκBα were examined with Western blotting, NF-κB p65 nuclear translocation was analyzed with immunofluorescence assay, and MCP-1 expression in the supernatant was determined using ELISA kits. RESULTS: The medicated rat serum time- and concentration-dependently promoted the proliferation of MPC5, with the optimal serum concentration of 5% and incubation time of 24 h. AOPP significantly increased MCP-1 expression in the cell supernatant in a time-and concentration-dependent manner; pretreatment with SB203580 (a p38 inhibitor) or parthenolide (a NF-κB inhibitor) significantly decreased MCP-1 expression, and treatment with the medicated serum significantly decreased AOPP-induced MCP-1 expression. AOPP concentration-dependently increased the protein expression of P-p38 but decreased that of IκBα. Both the medicated serum and SB203580 increased IκBα protein in AOPP-induced cells, but the effect was more obvious with the medicated serum. The medicated serum also decreased NF-κB p65 nuclear translocation in AOPP-induced MPC5. CONCLUSION: Shenkang pill-medicated serum can decrease AOPP-induced expression of MPC-1 in MPC5 by regulating p38MAPK/NF-κB to mediate its anti-inflammatory effect. This finding provides a new theoretical basis for the application of Shenkang pill to treat diabetic nephropathy.
Assuntos
Produtos da Oxidação Avançada de Proteínas/farmacologia , Quimiocina CCL2/metabolismo , Medicamentos de Ervas Chinesas/farmacologia , Fator de Transcrição RelA/metabolismo , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo , Animais , Linhagem Celular , Proliferação de Células , Regulação para Baixo , Proteínas I-kappa B/metabolismo , Imidazóis , Camundongos , Inibidor de NF-kappaB alfa , Piridinas , Ratos , Soro/química , SesquiterpenosRESUMO
Diabetic nephropathy (DN) is one of the most common and serious chronic complications of diabetes mellitus, however, no efficient clinical drugs exist for the treatment of DN. We selected and synthesized several sesquiterpene lactones (SLs), and then used the MTT assay to detect rat mesangial cells (MCs) proliferation, ELISA to measure the expression level of monocyte chemoattractant protein-1 (MCP-1), transforming growth factor beta (TGF-ß1) and fibronectin(FN), real-time fluorescent quantitative PCR analysis to measure the MCP-1 and TGF-ß1 gene expression, western blot to detect the level of IκBα protein and EMSA to measure the activation of nuclear factor kappa B (NF-κB). We discovered that SLs, including parthenolide (PTL), micheliolide (MCL), arglabin, and isoalantolactone (IAL), as well as several synthetic analogs of these molecules, could effectively attenuate the high glucose-stimulated activation of NF-κB, the degradation of IκBα, and the expression of MCP-1, TGF-ß1 and FN in rat mesangial cells (MCs). These findings suggest that SLs and their derivatives have potential as candidate drugs for the treatment of DN.
Assuntos
Quimiocina CCL2/metabolismo , Glucose/fisiologia , Lactonas/farmacologia , Células Mesangiais/metabolismo , NF-kappa B/metabolismo , Sesquiterpenos/farmacologia , Fator de Crescimento Transformador beta1/metabolismo , Animais , Proliferação de Células/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Quimiocina CCL2/genética , Nefropatias Diabéticas/tratamento farmacológico , Avaliação Pré-Clínica de Medicamentos , Expressão Gênica/efeitos dos fármacos , Regulação da Expressão Gênica/efeitos dos fármacos , Lactonas/síntese química , Células Mesangiais/efeitos dos fármacos , Ligação Proteica , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Ratos , Espécies Reativas de Oxigênio/metabolismo , Sesquiterpenos/síntese química , Fator de Crescimento Transformador beta1/genéticaRESUMO
OBJECTIVE: To explore the effects of parthenolide (PTL) on high glucose-stimulated cell proliferation, NF-κB activation and monocyte chemoattractant protein-1 (MCP-1) expression in rat mesangial cells (MCs). METHODS: MCs were cultured in normal glucose (5.6 mmol/L), high glucose (30 mmol/L), or high glucose with PTL. MTT assay was used to detect the cell proliferation. MCP-1 content in the supernatant was measured by ELISA, and the level of IκBα was detected by Western blotting to reflect NF-κB activity. EMSA method was used to measure the activation of NF-κB. RESULTS: MC proliferation, MCP-1 expression and NF-κB activation were significantly enhanced and the expression of NF-κB-binding protein IκBα was obviously reduced in cells cultured in high glucose. Application of PTL obviously abolished the effects of high glucose. CONCLUSION: PTL can suppress high glucose-stimulated NF-κB activation and MCP-1 expression in rat MC. These data provide a theoretical basis for the clinical application of PTL in prevention and control of diabetic nephropathy.
Assuntos
Proliferação de Células/efeitos dos fármacos , Quimiocina CCL2/metabolismo , Células Mesangiais/citologia , NF-kappa B/antagonistas & inibidores , Sesquiterpenos/farmacologia , Animais , Anti-Inflamatórios não Esteroides/isolamento & purificação , Anti-Inflamatórios não Esteroides/farmacologia , Asteraceae/química , Células Cultivadas , Relação Dose-Resposta a Droga , Glucose/administração & dosagem , Glucose/farmacologia , Proteínas I-kappa B/metabolismo , Células Mesangiais/metabolismo , Inibidor de NF-kappaB alfa , NF-kappa B/metabolismo , Plantas Medicinais/química , Ratos , Sesquiterpenos/isolamento & purificaçãoRESUMO
The Cathepsin L-like cysteine proteinase genes (cpls) are multifunction genes related to the parasitic abilities of plant parasitic nematodes. A new cathepsin L-like cysteine proteinase gene (Dd-cpl-1) (GenBank Accession GQ 180107) was cloned from Ditylenchus destructor by RT-PCR and RACE. The cDNA sequence consisted of a 1 131 bp open reading frame (ORF) encoding 376 amino acid residues that were franked by a 29 bp 5'-untranslated region (UTR) and a 159 bp 3'-UTR. Genomic sequence analysis showed that Dd-cpl-1 contained 7 introns, obeyed the GT/AG rule in the splice-site junctions. Homology analysis showed that the identity was 77% between Dd-cpl-1 deduced protein Dd-CPL-1 and cathepsin L-like cysteine proteinase of Bursaphelenchus xylophilus. Multi-sequence alignment indicated that there were the catalytic triad (Cys183, His322 and Asn343) and two motifs ERFNIN motif and GNFD motif in deduced protein Dd-CPL-1. Cysteine proteinases phylogenetic analysis showed that Dd-cpl-1 belonged to the sub-clade of cathepsin L-like cysteine proteinases.
Assuntos
Catepsina L/genética , Cisteína Proteases/genética , Genes de Helmintos/genética , Nematoides/enzimologia , Solanum tuberosum/parasitologia , Sequência de Aminoácidos , Animais , Clonagem Molecular , Dados de Sequência Molecular , Nematoides/genética , Filogenia , Alinhamento de Sequência , Análise de Sequência de Proteína , Homologia de Sequência de AminoácidosRESUMO
OBJECTIVE: To investigate the effects of Shenkangwan on the expressions of angiotensin II (AngII) and its type I receptor (AT(1)R) and the renalprotection mechanism of Shenkangwan in rats with early diabetic nephropathy (DN). METHODS: The rat models of DN established by a single injection of streptozotocin were randomly divided into 4 groups, namely the model group, Shenkangwan treatment group, irbesartan treatment group, and Shenkangwan and irbesartan treatment group, with normal rats as the control. All the rats received daily gavage for 8 weeks. The urinary protein quality in 24 h and plasma and renal contents of AngII were measured. The expressions of AT1R at the protein and mRNA levels in the kidney tissues were measured by immunohistochemistry and reverse transcription-polymerase chain reaction, respectively. The pathological changes of the kidney were observed microscopically. RESULTS: In DN rats, Shenkangwan reduced the urinary protein quantity in 24 h and the contents of AngII in the plasma and kidney tissues, decreased the renal expressions of AT(1)R protein and mRNA, and alleviated the morphological damage of the kidney. CONCLUSIONS: Shenkangwan offers renalprotection against DN probably by reducing the contents of AngII in the plasma and kidney tissues and inhibiting renal AT(1)R expressions.
Assuntos
Angiotensina II/metabolismo , Nefropatias Diabéticas/tratamento farmacológico , Medicamentos de Ervas Chinesas/uso terapêutico , Fitoterapia , Receptor Tipo 1 de Angiotensina/metabolismo , Angiotensina II/genética , Bloqueadores do Receptor Tipo 1 de Angiotensina II/uso terapêutico , Animais , Nefropatias Diabéticas/metabolismo , Rim/metabolismo , Masculino , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Ratos , Ratos Sprague-Dawley , Receptor Tipo 1 de Angiotensina/genéticaRESUMO
OBJECTIVE: To investigate the effects of alpha-keto acid on the expression of neuropeptide Y in malnutrition rats with chronic renal failure. METHODS: SD rats received 5/6 nephrectomy and were fed with 4% casein to establish models of malnutrition with chronic renal failure. Serum albumin, urea nitrogen, serum creatinine, type-1 insulin like growth factor and body weight of the rats were measured. The rat models were randomized into chronic renal failure group, alpha-keto acid group and normal control group, and after a 4-week treatment as indicated, neuropeptide Y mRNA levels in the hypothalamus were measured by RT-PCR in rats with surgically induced renal failure (two-stage subtotal nephrectomy). The blood neuropeptide Y of the rats were analyzed by radioimmunoassay. RESULTS: Malnutrition occurred in chronic renal failure rats at the end of 10 weeks. Compared with those in the chronic renal failure group, the plasma neuropeptide Y concentrations in alpha-keto acid group were significantly lowered with substantially elevated neuropeptide Y mRNA expression in the hypothalamus. CONCLUSION: alpha-keto acid capsule can improve malnutrition in rats with renal insufficiency possibly by up-regulating neuropeptide Y mRNA expression in the hypothalamus and reducing the level of blood neuropeptide Y.
Assuntos
Cetoácidos/farmacologia , Falência Renal Crônica/sangue , Desnutrição/tratamento farmacológico , Neuropeptídeo Y/sangue , Animais , Hipotálamo/metabolismo , Cetoácidos/uso terapêutico , Masculino , Desnutrição/sangue , RNA Mensageiro/genética , Ratos , Ratos Sprague-DawleyRESUMO
OBJECTIVE: To investigate the morphological changes and expressions of desmin and podocin in podocytes of rats with diabetic nephropathy (DN) rats and renal protection mechanism of Shenkangwan. METHODS: DN model was established in rats by a single injection of streptozotocin. The rats were then randomly divided into model group, Shenkangwan treatment group, irbesartan treatment group, and Shenkangwan plus irbesartan treatment group, with normal rats as the control group. All the rats received daily gavage for 8 weeks. The urinary protein quantity in 24 h were detected, and the morphological changes of the kidneys were observed with optic and transmission electron microscopes. The expressions of desmin and podocin in the podocytes were detected by immunohistochemistry. RESULTS: Shenkangwan and irbesartan reduced the urinary protein quantity in 24 h and alleviated the renal damage in DN rats, and the expression of desmin was significantly attenuated while podocin expression increased in the podocytes. CONCLUSIONS: Shenkangwan can provide renal protection against DN in rats and alleviate the structural and functional damages of podocytes possibly by reducing desmin expression and increasing podocin expression in the podocytes.
Assuntos
Nefropatias Diabéticas/tratamento farmacológico , Medicamentos de Ervas Chinesas/farmacologia , Podócitos/efeitos dos fármacos , Animais , Desmina/biossíntese , Nefropatias Diabéticas/patologia , Medicamentos de Ervas Chinesas/uso terapêutico , Imuno-Histoquímica , Rim/efeitos dos fármacos , Rim/patologia , Rim/ultraestrutura , Masculino , Microscopia Eletrônica de Transmissão , Fitoterapia , Podócitos/metabolismo , Podócitos/patologia , Distribuição Aleatória , Ratos , Ratos Sprague-DawleyRESUMO
OBJECTIVE: To investigate the effects of Shenkang pill on renal function and extracellular matrix secretion on the diabetic rats. METHOD: The diabetic rat models were induced by intraperitoneal injection of streptozotocin (STZ) and randomly divided into 3 groups' model control group; Capoten group and Shenkangwan group. Some normal other rats were used as normal control group. All rats were treated with corresponding drugs for 8 weeks. During and after the treatment, the general state, blood and urine glucose levels, excretion rate of the 24 hour urine protein and albumin, serum creatinine and blood urea nitrogen contents, kidney weight and relative kidney weight were measured. The mRNA of fibronectin(FN) in the kidney also detected by semi-quantitative reverse transcription polymerase chain reaction(RT-PCR). RESULT: Diabetes mellitus and renal lesions occurred in the three model groups. The expression of FN mRNA of the kidney in diabetic rats increased obviously. Shenkang pill could improve the general state and renal function of the diabetic rats, decrease the blood glucose levels and the excretion rate of the 24 hour urine protein and albumin, reduce the expression of FN mRNA in kidney. CONCLUSION: Shenkang pill has a certain protective effect on the diabetic kidney.
Assuntos
Nefropatias Diabéticas/metabolismo , Medicamentos de Ervas Chinesas/farmacologia , Fibronectinas/biossíntese , Plantas Medicinais , Animais , Glicemia/metabolismo , Nitrogênio da Ureia Sanguínea , Nefropatias Diabéticas/induzido quimicamente , Nefropatias Diabéticas/patologia , Combinação de Medicamentos , Medicamentos de Ervas Chinesas/isolamento & purificação , Fibronectinas/genética , Hemoglobinas Glicadas/metabolismo , Rim/metabolismo , Masculino , Plantas Medicinais/química , RNA Mensageiro/biossíntese , RNA Mensageiro/genética , Distribuição Aleatória , Ratos , Ratos Wistar , EstreptozocinaRESUMO
OBJECTIVE: To study the mechanism of Shenkangwan (SKW) in treating early diabetic nephropathy (DN). METHODS: The effect of SKW on NO and transforming growth factor (TGF)-beta(1) production by the mesangial cells (MCs) of rats with early diabetic nephropathy was evaluated with serum pharmacological method. RESULTS: Compared with normal serum, the SKW-containing serum dose- and time-dependently inhibited TGF-beta(1) excretion and increased NO production in the MCs of rats with early DN (P<0.05 and P<0.01, respectively). CONCLUSION: The therapeutic effect of SKW on early DN may rely on the balance modulation of cytokine network by increasing NO production and decreasing TGF-beta(1) excretion to prevent cytokine-induced damage of the MCs.