Protective effect of sakuranetin in brain cells of dementia model rats.

Alzheimer's disease (AD) is a high-incidence neurodegenerative disease with complex and diverse pathogenesis. With aging of the population and continuous improvement of living standards, the incidence of AD is on the increase. Therefore, there is need to develop more effective AD drugs in order to improve the quality of life of the elderly. Sakuranetin (SAK) is a dihydroflavonoid compound extracted from plants. It has many physiological properties. In this study, the effect of SAK on spatial discrimination in a rat model of cognitive dysfunction exposed to D-galactose was investigated with respect to its effect on malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels, and on the expressions of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and nuclear factor-κB inhibitory factor-α (IκBα) in hippocampus of rats. The results obtained suggest that SAK may exert protective effects on brain cells through anti-oxidation mechanism. Moreover, the improvement in learning and memory impairment by SAK may also be related to the inhibition of inflammatory mediators in brain tissue. These findings provide scientific evidence that can be exploited for more effective treatment of Alzheimer's disease.

[Effects of Qufengtongluo Recipe on podocin mRNA expression and podocyte morphology in rats with adriamycin-induced nephropathy].

OBJECTIVE: To observe the effects of Qufengtongluo Recipe (QFTLR) on the expression of podocin mRNA and podocyte morphology in rats with adriamycin-induced nephropathy (AN), and explore the possible mechanism mediating the therapeutic effect of QFTLR on nephropathic proteinuria. METHODS: SD rats were randomized into normal control group, AN model group (established by a single injection of adriamycin via the tail vein), and 3 intervention groups with QFTLR, prednisone, or benazepril treatment. After the corresponding treatments, the expression of podocin mRNA in the renal tissues was detected by RT-PCR methods, and the morphological changes of the podocytes were examined by electron microscope. RESULTS: Compared with the normal control group, the AN model group showed significantly lowered expressions of podocin mRNA (P<0.01) with reduced podocytes and widening, fusion or even absence of the foot processes (FP). Intervention with QFTLR significantly increased the expression of podocin mRNA (P<0.01) and the number of podocytes, and obviously lessened the structural changes of the FP. CONCLUSION: QFTLR can produce therapeutic effect against nephropathic proteinuria possibly by up-regulating the expression of podocin mRNA and improving the morphological changes of the podocytes.

[Effects of Qufengtongluo recipe on proteinuria and glomerular filtration membrane in rats with adriamycin-induced nephropathy].

OBJECTIVE: To assess the therapeutic effect of Qufengtongluo (QFTL) recipe against proteinuria and glomerular filtration membrane damage in rats with adriamycin-induced nephropathy (AN). METHODS: Fifty-six SD rats were randomized into normal control (A) and AN model groups. In the AN model group, the rat AN models established by a single intravenous injection of adriamycin via the tail vein were subdivided into model (B), QFTL recipe (C), prednisone (D), and benazepril (E) groups 3 weeks after adriamycin injection. The 24-h urinary protein level was measured and the expression of anionic sites on the filtration membrane was evaluated using electron microscope with PEI staining. Nephrin expression on the glomerular filtration membrane was detected with indirect immunofluorescence assay. RESULTS: Compared with group A, the model group showed significantly increased level of 24-h urinary protein (P<0.01), suggesting successful establishment of the AN model. Treatment with QFTL recipe obviously lowered the 24-h urinary protein (P<0.01), and increased the expression of anionic sites and nephrin on the glomerular filtration membrane in the AN rats (P<0.01). CONCLUSION: QFTL recipe can effectively decrease 24-h urinary protein, improve the symptoms, and up-regulate the expressions of anionic sites and nephrin on the glomerular filtration membrane in rats with AN.

[Effects of qufengtongluo recipe on expressions of HSPG mRNA and protein in adriamycin-induced nephropathy rats].

OBJECTIVE: To investigate the expression of HSPG in glomerular base membrane of adriamycin-induced nephropathy (AN) rats, and the effect of Qufengtongluo recipe on HSPG mRNA expression and proteinuria in AN rats. METHODS: One hundred forty rats were used in this study, including 32 rats in normal control group. AN was induced in the left rats by a single tail intravenous injection of adriamycin. Three weeks later, 90 AN rats were randomly divided into five groups; the nephropathy group (B, n=18), the Qufeng group (C, n=18), Qufeng and prednisone group (D, n=18), prednisone group(E,n=18) and benazepri group (F, n= 18). The rats in these five groups were treated with different combination of Qufeng recipe and prednisone. In each group, renal tissue samples were collected at week 3 and 7. The distribution, expression of HSPG was examined by indirect immunofluorescence, and semi-quantity RT-PCR, respectively. RESULTS: (1) In AN rats, the diffuse fusion and effacement of foot processes were observed when model established. (2) Compared with nephropathy group, the average fluorescence intensity of HSPG dramatically increased in Qufeng group and prednisone group (P < 0.01), similarly, it also increased in D and F groups (P < 0.01). (3) Compared with nephropathy group, the expression of HSPG mRNA was significantly up-regulated in other groups. (P < 0.01), especially in C and F groups. There was significant negative correlation between the expression of HSPG and quantity of 24-hour proteinuria. CONCLUSION: The abnormal expression of HSPG and their altered distributions may be an important molecular mechanism that leads to the occurrence and development of proteinuria in AN rats. The effect of Qufengtongluo recipe on nephrotic syndrome might be related to the alteration of HSPG expression and distribution in glomerulus.

[Effect of Qufengtongluo recipe on expression of nephrin mRNA in adriamycin-induced nephropathy in rats].

OBJECTIVE: To investigate the expression of nephrin mRNA in adriamycin-induced nephropathy (AN) in rats, and to explore the effect of Qufengtongluo recipe on proteinuria in AN rats and on the expression of nephrin mRNA. METHODS: Adriamycin nephropathy was induced by a single tail intravenous injection of adriamycin. We randomly divided 140 rats into a normal control group (n=32) and a nephropathy model group (n=108). Three weeks later, 90 AN rats were randomly divided into 5 groups: a model group, a qufeng group, a qufeng and prednisone group, a prednisone group, and a benazepri group (18 rats in each group). They were treated respectively, and renal tissue samples were collected at week 0, 3, 5, and 7, respectively. The distribution and expression of nephrin mRNA were examined by indirect immunofluorescence and semi-quantity RT-PCR. RESULTS: In the AN rats, the diffuse fusion and effacement of foot processes were observed at week 3. The fluorescence intensity of nephrin and the expression of nephrin mRNA significantly increased in the qufeng group and the prednisone group compared with the model group at the week 7 (P<0.01). CONCLUSION: Abnormal expression of nephrin is the important molecular mechanism that leads to the occurrence and development of proteinuria in AN rats. Qufengtongluo recipe has effect on nephrotic syndrome through altering the expression and distribution of nephrin in glomerulus.

[Qufeng Tongluo decoction inhibits lipopolysaccharide-induced rat mesangial cell proliferation in vitro by suppressing NF-kappaB activation and reducing TGF-beta1 and IL-6 mRNA expressions].

OBJECTIVE: To investigate the effect of Qufeng Tongluo (QFTL) decoction on lipopolysaccharide (LPS)-induced rat mesangial cell proliferation and explore the possible mechanisms underlying the therapeutic effects. METHODS: Thirty-two rats were randomized into normal control, glomerulonephritis model, QFTL treatment and positive control groups, and serum samples were obtained from these groups. Rat mesangial cells with or without LPS exposure were treated with the sera, and the expression of nuclear factor-kappaB (NF-kappaB ) was detected using electrophoretic mobility shift assay (EMSA), and the expressions of transforming growth factor-beta1 (TGF-beta1) and interleukin-6 (IL-6) mRNAs were detected with RT-PCR. RESULTS: QFTL decoction inhibited the activation of NF-kappaB in LPS-stimulated rat mesangial cells stimulated by LSP, and lowered the expressions of TGF-beta1 and IL-6 mRNA. CONCLUSION: QFTL decoction can inhibit LPS-induced rat mesangial cell proliferation by decreasing the expression of TGF-beta1 and IL-6 mRNA as a result of suppression NF-kappaB activation.

[Effects of Qufeng Tongluo Recipe on proliferation of and TGF-beta1 and IL-6 mRNA expressions in glomerular mesangial cells from rats].

OBJECTIVE: To investigate the effects of Qufeng Tongluo Recipe (QFTLR), a compound of traditional Chinese herbal medicine for dispelling wind and removing obstruction in the meridians, on cell proliferation and expressions of transforming growth factor-beta1 (TGF-beta1) and interleukin-6 (IL-6) mRNAs induced by lippolysaccharide in glomerular mesangial cells from rats. METHODS: The method of serum pharmacology was used. A total of 32 rats were divided into normal control group, untreated group, QFTLR group and positive control group which also was named Monopril (fosinopril sodium) group. Mesangial proliferative glomerulonephritis was induced by injection of antithymocyte serum in the rats except for the normal control group. Sera of the rats were obtained after corresponding interventions. Lipopolysaccharide-induced proliferation of rat mesangial cells (MCs) cultured in the respective serum-containing media was detected by the method of methyl thiazolyl tetrazolium (MTT) assay, and the expressions of TGF-beta1 and IL-6 mRNAs were analyzed by the method of reverse transcription polymerase chain reaction. RESULTS: Compared with the untreated group, QFTLR showed remarkable inhibitory function on the proliferation of the mesangial cells (P<0.05). The expressions of TGF-beta1 mRNA in mesangial cells were increased in the untreated group, QFTLR group and Monopril group when compared with the normal control group (P<0.01), but the TGF-beta1 mRNA expressions in QFTLR group and in Monopril group were lower than that in the untreated group. The IL-6 mRNA expression could be increased by the LPS stimulation, and it was significantly higher in the other three groups than that in the normal control group, including the untreated group, the Monopril group and the QFTLR group (P<0.01). Compared with the untreated group, the expression of IL-6 mRNA was decreased by QFTLR and Monopril (P<0.01). QFTLR was better than Monopril in inhibiting the proliferation of the mesangial cells and decreasing the expressions of TGF-beta1 and IL-6 mRNAs (P<0.05). CONCLUSION: QFTLR has great inhibitory effect on mesangial cell proliferation and expressions of TGF-beta1 and IL-6 mRNAs, which may be one of its mechanisms in postponing glomerular sclerosis.

Study on effect of yishen capsule in preventing recurrence of chronic glomerulonephritis.

OBJECTIVE: To observe the effect of yishen capsule (YSC) on preventing the recurrence of chronic glomerulonephritis (CGN) and to explore its mechanism preliminarily. METHODS: CGN patients were assigned to the treated group (61 cases) and the control group (48 cases) and all of them were orally administered with 4 mg of Perindopril twice a day, but 3 capsules of YSC, thrice a day, were given additionally to patients in the treated group. The therapeutic course for both groups was 18 months. The recurrence rate of CGN at the 6th, 12th, and 18th month in the two groups was observed and compared, and the changes of 24-h urinary protein quantity and T-lymphocyte subsets before and after treatment were observed as well. RESULTS: (1) Comparison of recurrence rate between the two groups showed insignificant difference at the 6th month, but it did show significant difference at the 12th and the 18th month, which was significantly decreased in the treated group than in the control group (P<0.05, P<0.01); (2) The 24-h urinary protein quantity at the 18th month decreased significantly in both groups (P<0.05, P<0.01), but in the treated group was more significant (P<0.01); (3) T-lymphocyte subsets showed no obvious change in the control group after treatment (P>0.05), while in the treated group, it showed significant increase in CD3, CD4 and CD4/CD8 (P<0.05 or P<0.01) and significant decrease in CD8 (P<0.05), and also the difference after treatment in T-lymphocyte subsets between the two groups was significant (P<0.05 or P<0.01). CONCLUSION: YSC has marked effects in reducing the recurrence of CGN and in decreasing urinary protein, and its mechanism might be related with its function in regulating the ratio of T-lymphocyte subsets to enhance the immunity of patients.