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1.
J Huazhong Univ Sci Technolog Med Sci ; 37(1): 25-29, 2017 Feb.
Article in English | MEDLINE | ID: mdl-28224432

ABSTRACT

The traditional Chinese medicine (Tripterygium wilfordiiHook.f., TWH) has been clinically used to treat primary and secondary renal diseases and proteinuria for nearly 40 years. However, there is a rare literature about the effect of triptolide (the main active ingredient of TWH) on the expression of oxidative carbonyl protein (OCP) in diabetic nephropathy (DN). This study aimed to provide experimental evidence for triptolide treatment on DN through its effect on the expression of OCP, in order to investigate the effects of triptolide on the expression of OCP in rats with DN. Sixty SD rats were randomly divided into five groups: control group, high-dose triptolide (Th) group, low-dose triptolide (Tl) group, DN model group, and positive control (benazepril) group. The DN model was established using streptozotocin. Urinary protein excretion, fasting blood glucose (FBG), superoxide dismutase (SOD) in renal homogenate, malondialdehyde (MDA) in renal homogenate and renal nitrotyrosine by immunohistochemistry, and the expression of OCP by oxyblotimmune blotting were detected. In the DN model group, rat urinary protein excretion and renal MDA were significantly increased, while renal SOD significantly decreased and nitrotyrosine expression was obviously upregulated in the kidney. After triptolide treatment, 24-h urinary protein excretion (61.96±19.00 vs. 18.32±4.78 mg/day, P<0.001), renal MDA (8.09±0.79 vs. 5.45±0.68 nmol/L, P<0.001), and nitrotyrosine expression were decreased. Furthermore, renal OCP significantly decreased, while renal SOD (82.50±19.10 vs. 124.00±20.52 U/L, P<0.001) was elevated. This study revealed that triptolide can down-regulate the expression of OCP in the renal cortex of DN rats.


Subject(s)
Diabetic Nephropathies/drug therapy , Diterpenes/administration & dosage , Drugs, Chinese Herbal/administration & dosage , Kidney Cortex/metabolism , Phenanthrenes/administration & dosage , Protein Carbonylation/drug effects , Streptozocin/adverse effects , Animals , Blood Glucose/metabolism , Diabetic Nephropathies/chemically induced , Diabetic Nephropathies/metabolism , Disease Models, Animal , Diterpenes/pharmacology , Drugs, Chinese Herbal/pharmacology , Epoxy Compounds/administration & dosage , Epoxy Compounds/pharmacology , Gene Expression Regulation/drug effects , Humans , Oxidative Stress , Phenanthrenes/pharmacology , Proteins/metabolism , Random Allocation , Rats , Rats, Sprague-Dawley , Superoxide Dismutase/metabolism
2.
Zhongguo Zhong Xi Yi Jie He Za Zhi ; 37(2): 155-159, 2017 Feb.
Article in Chinese | MEDLINE | ID: mdl-30650265

ABSTRACT

Objective To observe the clinical effect of Jinchuang Ointment (JO) for treatment of refractory pressure ulcers. Methods Totally 306 patients with phase II , IIl, IV refractory pressure ul- cers were randomly assigned to the traditional Chinese herbal medicine ointment group, the JO group, the MepilexAg group,102 cases in each group. Each ulcer was scored using pressure ulcer scale for healing (PUSH) designed by National Pressure Ulcer Advisory Panel (NPUAP) before treatment, at day 7, 14, and 21 after treatment, respectively. The healing rate of pressure ulcer was observed at day 21. Results There was significant difference in PUSH score of the 3 groups between before treatment and at day 7/14)21 after treatment (P <0. 01). PUSH score was better in the JC group, as compared with that in the other two groups (P <0. 05) at day 14 and 21 after treatment. There was no significant difference in PUSH score between the traditional Chinese herbal medicine ointment group and the MepilexAg group (P >0. 05). Conclusions JO had significant effect in treatment of patients with phase II , III, IV pressure ulcers. The rate of wound healing at day 14/21 was significantly higher than that of traditional Chinese herbal medicine ointment and MepilexAg.


Subject(s)
Medicine, Chinese Traditional , Ointments , Pressure Ulcer , Humans , Pressure Ulcer/therapy , Wound Healing
3.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-238394

ABSTRACT

The traditional Chinese medicine (Tripterygium wilfordiiHook.f.,TWH) has been clinically used to treat primary and secondary renal diseases and proteinuria for nearly 40 years.However,there is a rare literature about the effect of triptolide (the main active ingredient of TWH) on the expression of oxidative carbonyl protein (OCP) in diabetic nephropathy (DN).This study aimed to provide experimental evidence for triptolide treatment on DN through its effect on the expression of OCP,in order to investigate the effects of triptolide on the expression of OCP in rats with DN.Sixty SD rats were randomly divided into five groups:control group,high-dose triptolide (Th) group,low-dose triptolide (T1) group,DN model group,and positive control (benazepril) group.The DN model was established using streptozotocin.Urinary protein excretion,fasting blood glucose (FBG),superoxide dismutase (SOD) in renal homogenate,malondialdehyde (MDA) in renal homogenate and renal nitrotyrosine by immunohistochemistry,and the expression of OCP by oxyblotimmune blotting were detected.In the DN model group,rat urinary protein excretion and renal MDA were significantly increased,while renal SOD significantly decreased and nitrotyrosine expression was obviously upregulated in the kidney.After triptolide treatment,24-h urinary protein excretion (61.96±19.00 vs.18.32±4.78 mg/day,P<0.001),renal MDA (8.09±0.79 vs.5.45±0.68 nmol/L,P<0.001),and nitrotyrosine expression were decreased.Furthermore,renal OCP significantly decreased,while renal SOD (82.50±19.10 vs.124.00±20.52 U/L,P<0.001) was elevated.This study revealed that triptolide can down-regulate the expression of OCP in the renal cortex of DN rats.

4.
J Huazhong Univ Sci Technolog Med Sci ; 35(3): 356-361, 2015 Jun.
Article in English | MEDLINE | ID: mdl-26072073

ABSTRACT

Diabetic nephropathy (DN) is a common and serious clinical complication of diabetes and presently there are no effective ways to prevent its occurrence and progression. Recent studies show that pentoxifylline (PTX) can improve renal hemodynamics, reduce urinary protein excretion, and alleviate or delay renal failure in DN patients. In this study, we focused on the anti-oxidative stress effect of PTX on alleviating renal damages of DN using rat models. DN rats were established with injection of streptozotocin. Blood glucose, urinary protein excretion, serum cystatin C, renal biopsy, superoxide dismutase (SOD) and malondialdehyde (MDA) in serum and renal homogenate and renal nitrotyrosine levels were analyzed before and 12 weeks after the treatment of PTX. Before treatment, all the DN rats had elevated blood glucose, increased urinary protein excretion and elevated serum cystatin C. Morphologically, DN rats exhibited renal tissue damages, including swelling and fusions of foot processes of podocytes under electron microscope. Masson staining revealed blue collagen deposition in glomeruli and renal interstitium. With treatment of PTX, symptoms and renal pathological changes of DN rats were alleviated. Furthermore, the MDA levels were increased and the SOD levels were decreased in the serum and kidneys of DN rats, and these changes were reversed by PTX. The expression of nitrotyrosine was up-regulated in DN rat model and down-regulated by PTX, indicating that PTX was able to inhibit oxidative reactions in DN rats. PTX could alleviate renal damage in DN, which may be attributable to its anti-oxidative stress activity.


Subject(s)
Biomarkers/analysis , Diabetes Mellitus, Experimental/drug therapy , Diabetic Nephropathies/drug therapy , Oxidative Stress/drug effects , Pentoxifylline/administration & dosage , Animals , Diabetes Mellitus, Experimental/pathology , Diabetic Nephropathies/metabolism , Diabetic Nephropathies/pathology , Gene Expression Regulation/drug effects , Kidney/metabolism , Kidney/pathology , Malondialdehyde/blood , Pentoxifylline/pharmacology , Rats , Streptozocin , Superoxide Dismutase/metabolism , Tyrosine/analogs & derivatives , Tyrosine/metabolism
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