Pygeum africanum: Effect on oxidative stress in early diabetes-induced bladder
Institute of Experimental Nuclear Medicine, Shandong University School of Medicine, 44# Wenhua Xi Road, 250012, Jinan, Shandong, China. International Urology and Nephrology
(Impact Factor: 1.52).
07/2009; 42(2):401-8. DOI: 10.1007/s11255-009-9610-5
To evaluate the effect of Pygeum africanum on oxidative stress and functional changes of the bladder after diabetes induction.
Thirty-two adult Wistar male rats were treated daily for 8 weeks and grouped as follows: Control group (n = 6), Streptozotocin-induced diabetic group (n = 10), diabetes plus P. africanum group (n = 10), and control plus P. africanum group (n = 6). After diabetes induction for 4 weeks, the diabetes plus P. africanum and control plus P. africanum groups were fed with P. africanum (100 mg/kg, orally) in peanut oil for another 4 weeks. The catalase, superoxide dismutase activity, and malondialdehyde levels were measured as a marker of lipid peroxidation. The levels of inducible nitric oxide synthase were also evaluated. Urodynamic studies were performed to evaluate the functional changes of diabetic bladders after P. africanum treatment.
The catalase and superoxide dismutase activities significantly increased (P < 0.05) and maleic dialdehyde levels significantly decreased from diabetic plus P. africanum group compared with diabetic group (P < 0.05). Immunohistochemical studies showed a significantly decreased number of inducible nitric oxide synthase-positive cells in diabetic plus P. africanum group compared with diabetic group (P < 0.05). In diabetic plus P. africanum group, maximal bladder volume significantly decreased, while bladder pressure and maximal bladder pressure significantly increased compared with diabetic group (P < 0.05).
Early treatment with P. africanum could effectively suppress the oxidative stress status in diabetic bladder and may slow down the process of diabetic cystopathy.
Available from: Rong-Rong He
- "All these results demonstrated that restraint stress promoted oxidative damage by increasing radical production and suppressing radical clearance ability. Under oxidative stress, BPH-related growth factors such as basic fibroblast growth factor and transforming growth factor b would be stimulated and contributed to the progression of BPH (Wang et al., 2010). Accordingly, oxidative stress was indicated to play a key role in the mechanism responsible for restraint stress-provoked BPH. "
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ABSTRACT: Clinical research has revealed that stressed men are susceptible to develop benign prostatic hyperplasia (BPH). In this study, restraint-stress mice model was employed to mimic the physiological conditions of the population that was susceptible to develop BPH. Male mice were subjected to restraint stress after being subcutaneously injected with testosterone propionate (TP) for 14 cl. Results demonstrated that TP-induced BPH was significantly aggravated by restraint stress, as manifested by increases of prostate index, serum testosterone level, and prostate 5 alpha-reductase (5AR) and serum acid phosphatase (ACP) activities. These findings were further supported by results of prostate pathological examination. However, we found that anthocyanins extract (AE) from bilberry (Vaccinium myrtillus L.) had additive effect with pollen of Brassica napus L. (PBN), a widely used folk remedy for BPH in traditional Chinese medicine, on stress-provoked BPH in mice. The mechanism was associated with the protective effects of AS against stress-induced oxidative damage, as indicated by decreased lipid peroxidation level, increased oxygen radical absorbance capacity (ORAC) and glutathione (GSH) content, along with elevated superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities. Our results proved that-stress-induced oxidative damage promoted the development and aggravation of BPH, while antioxidative defense contributed to the amelioration of BPH.
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ABSTRACT: To evaluate the gene and protein expression of nerve growth factor (NGF) and substance P (SP) in the bladder 8 weeks after diabetes induction and investigate the pathogenesis of diabetic cystopathy.
Thirty Wistar rats were divided into three groups: control (n = 10), streptozotocin-induced diabetic group (n = 10) and Pygeum africanum (P. africanum) group (n = 10; diabetic rats were given P. africanum (100 mg/kg/day)). Eight weeks later, the bladders were dissected. We measured the expression of NGF and SP in the bladders using RT-PCR, ELISA and immunohistochemistry.
We found a significantly reduced expression of NGF in the bladders from the diabetic group compared with the control. Immunohistochemical studies showed a statistically significant reduction of SP in the bladders from the diabetic group compared with the control (P < 0.05). Expression of NGF was greatly increased in the P. africanum group compared with that of the diabetic group. Immunohistochemical studies showed an increased level of SP in the bladders from the P. africanum group compared with the control (P < 0.05).
Our findings indicated that the decrease in NGF and SP may be a contributory factor in diabetic cystopathy. In addition, P. africanum could significantly upregulate the expression of NGF and SP in diabetic rats.
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ABSTRACT: Partial bladder outlet obstruction (PBOO) in rabbits causes free radical production through ischemia and reperfusion within the bladder smooth muscle and mucosa. We had previously shown that pretreatment of rabbits with a combination of α-lipoic acid (αLA) and coenzyme Q10 (CoQ) protected the bladder from contractile and metabolic dysfunctions mediated by PBOO. In this study, we examined the ability of pretreatment with αLA and CoQ combination in rabbits to protect the bladder from contractile damage mediated by either hydrogen peroxide (H(2)O(2)) or in vitro ischemia-reperfusion (I/R) which represents two in vitro models of oxidative damage.
Eight adult male New Zealand white rabbits were pretreated with CoQ and αLA orally for four weeks. Eight adult male control rabbits were given vehicle. Eight full-thickness bladder strips were isolated from each of 4 treated and 4 control rabbit bladders, and a dose-response curve to H(2)O(2) (0.1-0.8%) was generated. Similarly, isolated strips of bladder from the remaining 4 control and 4 treated rabbits were subjected to 1 h of ischemia (no oxygen without glucose) followed by 2 h of incubation in oxygenated buffer with glucose. The effects on the contractile responses to field stimulation (FS) at 2, 8, and 32 Hz, carbachol, and potassium chloride (KCl) were determined.
H(2)O(2) reduced the contractile responses to KCl and carbachol to a significantly greater degree than to FS, whereas I/R reduced the contractile responses to FS to a significantly greater degree than to KCl and carbachol. Pretreatment of the rabbits with the combination of CoQ and αLA significantly protected the bladder from the damaging effects of I/R, but had virtually no effect on the damaging effects of H(2)O(2).
Although both H(2)O(2) and I/R are in vitro models of oxidative free radical damage to bladder smooth muscle, they have significantly different methods of action and different sensitivities to antioxidants.
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