Hexane fraction of Annona muricata (Sour sop) seed ameliorates testosterone-induced benign prostatic hyperplasia in rats.

BACKGROUND: Annona muricata is used in traditional African medicine to manage urinary obstruction. In this study, we hypothesized that hexane fraction of Annona muricata (HFAM) seeds will ameliorate testosterone propionate (Tp)-induced benign prostatic hyperplasia (BPh). METHODS: Castrated rats were assigned into six groups: non-castrated control, castrated control, castrated rats that received Tp (BPh group), [BPh+HFAM], [BPh+HFAM + finasteride], [BPh + finasteride]. RESULTS: The BPh rats had 3.8 and 3.9 folds increases in prostatic and organo-somatic weight, while treatment with HFAM alone and [HFAM + finasteride] decreased prostatic weight by 22% and 34%, respectively. BPh increased the activities of serum and prostatic total acid phosphatase by 95% and 121%; and activities of serum and prostatic alkaline phosphatase by 54% and 281%, respectively. Serum and prostatic lipid peroxidation were increased by 44% and 82%, respectively, in BPh rats with a concomitant decrease in prostatic superoxide dismutase by 73%. In BPh rats, serum and prostatic myeloperoxidase increased by 4.0 and 2.0 folds, while serum nitric oxide increased by 2.4 folds, respectively. Strong expression of inducible nitric oxide synthase, Bcl2, beta-catenin, androgen and estrogen receptors were observed in BPh rats. Importantly, treatment with HFAM or finasteride (or combination) attenuated prostatic weight, inflammatory and antioxidant indices in BPh rats. CONCLUSION: HFAM may serve as novel therapeutic agent against BPh.

Methyl jasmonate reduces testosterone-induced benign prostatic hyperplasia through regulation of inflammatory and apoptotic processes in rats.

BACKGROUND: Phytotherapy is becoming a treatment option in management of diseases including benign prostatic hyperplasia (BPH). We have shown previously that methyl jasmonate (MeJA) ameliorated BPH, however the underlying mechanism of action remains unknown. This study was designed to investigate in mechanistic terms the protective role of MeJA in BPH. METHODS: BPH was induced by daily injections of testosterone propionate (TP) (3mg/kg) for 28 days. RESULTS: The weight and organo-somatic weight of prostate in BPH rats were 6.8 and 5.1 times higher than castrated-control group, respectively. Inflammatory markers; prostatic myeloperoxidase and total nitric oxide were significantly increased in BPH group. The activity of aniline hydroxylase (Phase I drug metabolizing enzyme) was significantly increased in BPH rats by 22%. In BPH group, immuno-histochemistry revealed strong expression of prostatic inducible nitric oxide synthase, cyclooxygenase-2 and Bcl2, while mild expression of p53 and Bax were seen. Serum triglyceride and total cholesterol were significantly increased, while HDL-c was decreased in BPH. Interestingly, MeJA and finasteride (singly or combination) attenuated inflammatory indices and induced apoptotic parameters in BPH rats. CONCLUSION: MeJA protects against TP-induced BPH via mechanisms that involve anti-inflammation, induction of apoptosis and inhibition of phase I drug metabolizing enzyme.

Methyl Jasmonate Ameliorates Testosterone Propionate-induced Prostatic Hyperplasia in Castrated Wistar Rats.

Benign prostate hyperplasia (BPH) is a progressive disease that is related to age. Known therapeutic agents used in the treatment of BPH are associated with toxicity. Therefore, chemoprevention could be an effective approach. We investigated the ameliorative effects of methyl jasmonate (MeJA) in testosterone propionate (TP)-induced BPH in castrated rats. Castration was performed by removing both testes through the scrotum sack under ketamine anesthesia. Rats were assigned into seven groups of seven animals each: non-castrated control, castrated control, castrated rats that received TP, castrated rats that received TP and MeJA, castrated rats that received TP and finasteride, castrated rats that received MeJA, and castrated rats that received finasteride. Results indicate that BPH rats had significantly (p < 0.05) elevated prostate weight and relative weight of prostate relative to control. Also, BPH rats had significantly (p < 0.05) increased activities of prostatic acid and alkaline phosphatases, levels of zinc, and malondialdehyde. Further, levels of enzymic and non-enzymic antioxidative indices were significantly (p < 0.05) reduced in BPH. Histology of prostate revealed hyperplasia of transition lobe, increased expression of PSA, and Ki67 in BPH. Treatment with MeJA and finasteride attenuated the activities of the phosphatases and levels of antioxidants in BPH. Overall, MeJA ameliorates BPH via antioxidative mechanism. Copyright © 2017 John Wiley & Sons, Ltd.

Modulatory effects of methanol extract of Artocarpus altilis (Moraceae) on cadmium-induced hepatic and renal toxicity in male Wistar rats.

BACKGROUND: Cadmium (Cd) is an environmental risk factor with an established toxicity in animals. Therefore, natural antioxidants may be protective against Cd-toxicity. The study was designed to investigate the modulatory effects of methanol extract of Artocarpus altilis (AA) on oxidant-antioxidant balance and lipid profile in liver and kidney of Cd-exposed rats while quercetin (QE) served as standard. METHODS: Total phenolic content (TPC) and 2,2-diphenyl-1-picryldydrazyl (DPPH) radical scavenging activity of AA were assessed in vitro. In vivo, rats were orally treated with AA (200mg/kg) and QE (25mg/kg) daily for three weeks and challenged with two doses of Cd (1.5mg/kg, i.p.) in the last 72h. RESULTS: The TPC and DPPH scavenging effects of AA were high and comparable with catechin. Cd-intoxication significantly (p<0.05) increased the activities of serum alanine aminotransferase and levels of urea, total bilirubin and creatinine by 94%, 60%, 234% and 76%, respectively. Cd-exposure caused a significant increase (p<0.05) in serum and tissues total cholesterol, triglyceride, low-density lipoprotein-cholesterol and reduction in high-density lipoprotein-cholesterol levels. The levels of hepatic and renal antioxidant parameters: glutathione-s-transferase, superoxide dismutase and reduced glutathione were significantly (p<0.05) decreased in Cd-intoxicated rats with concomitant elevation of lipid peroxidation. Histopathological findings revealed necrosis and distortion of architecture of renal tissue and, periportal infiltration in hepatocytes of Cd-intoxicated rats. Pretreatment with AA and QE restored antioxidant status, lipid profile and attenuated the lesions in the tissues. CONCLUSIONS: Extract of A. altilis protects against Cd-induced liver and kidney dysfunction via antioxidant and radical scavenging activities.

In vitro studies to assess the antioxidative, radical scavenging and arginase inhibitory potentials of extracts from Artocarpus altilis, Ficus exasperate and Kigelia africana.

OBJECTIVE: To justify the use of Artocarpus altilis (A. altilis), Ficus exasperata (F. exasperata) and Kigelia africana (K. africana) in ethnomedicine for the treatment of several ailments and to evaluate the in vitro antioxidant, radical scavenging and arginase inhibitory potentials of these herbs and compared with catechin (Standard). METHODS: Antioxidant activities were determined by 2,2-diphenyl-1-picrylhydrazyl (DPPH), nitric oxide, hydrogen peroxide (H2O2) and hydroxyl (OH) radicals scavenging methods. The flavonoids and phenolics content, inhibition of arginase activity, Fe(2+)/ascorbate-induced lipid peroxidation (LPO) and reducing power were also determined. RESULTS: The A. altilis, F. exasperata and K. africana showed dose-dependent and significant scavenging of DPPH, H2O2 and OH radicals in vitro relative to catechin. The A. altilis and F. exasperata effectively scavenged DPPH radical with IC50 of 593 and 635 µg/mL and, OH radical with IC50 of 487 and 514 µg/mL, respectively. The DPPH and OH radicals scavenging activities followed the order A. altilis>F. exasperata>K. africana. In addition, A. altilis and F. exasperata significantly (P<0.05) inhibited LPO in a dose-dependent manner. The A. altilis extract had the most potent inhibitory activity against LPO with 79% relative to catechin (28%) at 750 µg/mL. The reducing power followed the order: A. altilis>Catechin>F. exasperata>K. africana at 1 000 µg/mL. The A. altilis at 500 and 750 µg/mL significantly (P<0.05) inhibited arginase activity by 63% and 67%, respectively. The flavonoids contents were found to be highest in A. altilis. CONCLUSIONS: Extracts of A. altilis and F. exasperata are potent antioxidative agents with strong radical scavenging activity and inhibition of lipid peroxidation.

Effects of Methanol Extract of Breadfruit (Artocarpus altilis) on Atherogenic Indices and Redox Status of Cellular System of Hypercholesterolemic Male Rats.

We investigated the effects of methanol extract of Artocarpus altilis (AA) on atherogenic indices and redox status of cellular system of rats fed with dietary cholesterol while Questran (QUE) served as standard. Biochemical indices such as total cholesterol (TC), triglycerides (TG), low- and high-density lipoproteins-cholesterol (LDL-C and HDL-C), aspartate and alanine aminotransferases (AST and ALT), lactate dehydrogenase (LDH), reduced glutathione, glutathione-s-transferase, glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), and lipid peroxidation (LPO) were assessed. Hypercholesterolemic (HC) rats had significantly increased relative weight of liver and heart. Dietary cholesterol caused a significant increase (P < 0.05) in the levels of serum, hepatic, and cardiac TC by 110%, 70%, and 85%, LDL-C by 79%, 82%, and 176%, and TG by 68%, 96%, and 62%, respectively. Treatment with AA significantly reduced the relative weight of the organs and lipid parameters. There were beneficial increases in serum and cardiac HDL-C levels in HC rats treated with AA. In HC rats, serum LDH, ALT, and AST activities and levels of LPO were increased, whereas hepatic and cardiac SOD, CAT, and GPx were reduced. All biochemical and histological alterations were ameliorated upon treatment with AA. Extract of AA had protective effects against dietary cholesterol-induced hypercholesterolemia.