Protective effect of Cassia occidentalis extract on chemical-induced chromosomal aberrations in mice.

This study was conducted to determine the antimutagenic potential of aqueous extract of Cassia occidentalis against the chromosomal aberrations (CA) produced in vivo by benzo[a]pyrene (B[a]P) and cyclophosphamide (CP) in mice. Animals (male mice) were treated with three doses of plant extract (50 mg/kg, 250 mg/kg and 500 mg/kg) for 7 days prior to the administration of single dose of mutagens (B[a]P 125 mg/kg oral; CP 40 mg/kg i.p.). The results indicated that C. occidentalis was not genotoxic per se and exerted no other toxic signs and symptoms in treated animals. The chromosomal aberrations produced by B[a]P and CP were significantly reduced (p < 0.001) by C. occidentalis pre-treatment. Furthermore, animals treated with plant extract showed a reduced level of cytochrome P 450 (Cyt P 450) and elevated levels of glutathione S-transferase (GST) activity and glutathione content in the liver. It seems that C. occidentalis exerts its antimutagenic activity by modulating the xenobiotic activation and detoxification mechanisms.     

Protective Effect of Cassia Occidentals Extract on Chemical-Induced Chromosomal Aberrations in Mice

ABSTRACT

This study was conducted to determine the antimutagenic potential of aqueous extract of Cassia occidentalis against the chromosomal aberrations (CA) produced in vivo by benzo[a] pyrene (B[a]P) and cyclophosphamide (CP) in mice. Animals (male mice) were treated with three doses of plant extract (50mg/kg, 250mg/kg and 500mgAg) for 7 days prior to the administration of single dose of mutagens (B[a]P 125mg/kg oral; CP 40mg/kg i.p). The results indicated that C. occidentalis was not genotoxic per se and exerted no other toxic signs and symptoms in treated animals. The chromosomal aberrations produced by B[a]P and CP were significantly reduced (p < 0.001) by C. occidentalis pre-treatment. Furthermore, animals treated with plant extract showed a reduced level of cytochrome P 450 (Cyt P 450) and elevated levels of glutathione S-transferase (GST) activity and glutathione content in the liver. It seems that C. occidentalis exerts its antimutagenic activity by modulating the xenobiotic activation and detoxification mechanisms.     

Protective effect of Emblica officinalis ethanolic extract against 7,12-dimethylbenz(a) anthracene (DMBA) induced genotoxicity in Swiss albino mice

Ethanolic extract of Emblica officinalis (EO) fruit extract was evaluated for protection against genotoxicity induced by the rodent carcinogen, 7,12-dimethylbenz(a)anthracene (DMBA). Oral administration of EO fruit extract in various concentrations (100, 250, 500 mg/kg b.wt) for seven consecutive days prior to a single intraperitoneal injection of DMBA decreased the frequency of bone marrow micronuclei induced in Swiss albino mice. Significant increases in the liver antioxidants, such as glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR) and detoxifying enzyme glutathione-S-transferase (GST), were found in the fruit extract treated group. The extract also reduced the hepatic levels of the activating enzymes cytochrome (Cyt) P450 and Cyt b5. These increased in the carcinogen treated group, which emphasizes its protective effect against the carcinogen. There was a dose-dependent effect of the extract against the genotoxin with the maximum effect at 500 mg/kg b.wt. The protection afforded by EO may be associated with its antioxidant capacity and through its modulatory effect on hepatic activation and detoxifying enzymes.     

Protective effects of Emblica officinalis Gaertn. in cyclophosphamide-treated mice

Cyclophosphamide (CP) is one of the most popular alkylating anticancer drugs in spite of its toxic side effects including immunotoxicity, hematotoxicity, mutagenicity and a host of others. The present study was undertaken to assess the protective effects of total aqueous extract of a medicinal plant, Indian gooseberry (Emblica officinalis Gaertn.) in mice treated with CP. These protective effects were studied on immunological parameters and kidney and liver antioxidants. Plant extract treatment at a dose of 100 mg/kg body weight per os (p.o.) for 10 days resulted in the modulation of these parameters in normal as well as CP (50 mg/kg)-treated animals. Plant extract in particular was very effective in reducing CP-induced suppression of humoral immunity. Plant extract treatment in normal animals modulated certain antioxidants of kidney and liver. In CP-exposed animals, plant pretreatment provided protection to antioxidants of kidney. Not only were the reduced glutathione levels significantly (p<0.001) increased but plant extract treatment resulted in restoration of antioxidant enzymes in CP-treated animals. It is suggested that E. officinalis or its medicinal preparations may prove to be useful as a component of combination therapy in cancer patients under CP treatment regimen.     

Modulatory effects of gentisic acid against genotoxicity and hepatotoxicity induced by cyclophosphamide in Swiss albino mice

Objectives This study evaluated the protective effects of gentisic acid (GA) against genotoxicity and hepatotoxicity induced by cyclophosphamide (CP) in Swiss albino mice. Methods Mice were pretreated with GA orally at doses of 50 and 100 mg/kg for 14 consecutive days before the administration of a single intraperitoneal dose of 50 mg/kg CP. The ameliorative effect of GA on genotoxicity was studied using the in‐vivo bone marrow micronuclei induction test, DNA integrity and alkaline unwinding assay. The activity of various oxidative stress enzymes were estimated in hepatic tissue. Key findings A single intraperitoneal administration of CP in mice increased the malondialdehyde level, depleted the glutathione content and antioxidant enzyme activity (glutathione peroxidase, glutathione reductase, catalase and quinone reductase), and induced DNA strand breaks and micronuclei induction. Oral pretreatment with GA at both doses caused a significant reduction in malondialdehyde and glutathione levels, restoration of antioxidant enzyme activity, reduction in micronuclei formation and DNA fragmentation. Serum toxicity marker enzymes such as aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase were increased after CP treatment but restored in GA pretreated groups. Conclusion The results support the protective effect of GA against CP induced genotoxicity and hepatotoxicity.     

Emblica officinalis reverses thioacetamide-induced oxidative stress and early promotional events of primary hepatocarcinogenesis

Emblica officinalis is widely used in Indian medicine for the treatment of various diseases. In the present study, it was found that fruits of E. officinalis inhibit thioacetamide-induced oxidative stress and hyper-proliferation in rat liver. The administration of a single necrotic dose of thioacetamide(6.6 mM kg(-1)) resulted in a significant (P < 0.001) increase in serum glutamic oxaloacetic transaminase(SGOT), serum glutamic pyruvic transaminase (SGPT) and gamma-glutamyl transpeptidase (GGT) levels compared with saline-treated control values. Thioacetamide caused hepatic glutathione (GSH) depletion and a concomitant increase in malanodialdehyde (MDA) content. It also resulted in an increase(P < 0.001) in the activity of glutathione-S-transferase (GST), glutathione reductase (GR), glucose 6-phosphate dehydrogenase (G6PD) and a decrease in glutathione peroxidase (GPx) activity (P < 0.001). Hepatic ornithine decarboxylase activity and thymidine incorporation in DNA were increased bythioacetamide administration. Prophylactic treatment with E. officinalis for 7 consecutive days before thioacetamide administration inhibited SGOT, SGPT and GGT release in serum compared with treated control values. It also modulated the hepatic GSH content and MDA formation. The plant extract caused a marked reduction in levels of GSH content and simultaneous inhibition of MDA formation. E. officinalis also caused a reduction in the activity of GST, GR and G6PD. GPx activity was increased after treatment with the plant extract at doses of 100 mg kg(-1) and 200 mg kg(-1). Prophylactic treatment with the plant caused a significant down-regulation of ornithine decarboxylase activity (P < 0.001) and profound inhibition in the rate of DNA synthesis (P < 0.001). In conclusion, the acute effects of thioacetamide in rat liver can be prevented by pre-treatment with E. officinalis extract.     

Soy isoflavones inhibits the genotoxicity of benzo(a)pyrene in Swiss albino mice

Dietary factors are considered important environmental risk determinants for various diseases. Isoflavones are one of the biologically active polyphenolic plant constituents that possess potential chemopreventive properties against a wide variety of chronic diseases. In the present study we have evaluated the antimutagenic potential of soy isoflavones against benzo(a)pyrene (B[a]P) (125 mg/ kg) induced genotoxicity in Swiss albino mice. The effect of soy isoflavones was studied by in vivo bone marrow chromosomal aberration and micronuclei induction test. Using an alkaline unwinding assay we monitored the DNA strand breaks. Two doses of soy isoflavones (20 and 40 mg/kg b.wt) were given orally for seven days prior to the administration of B[a]P. Soy isoflavone inhibited the genotoxicity of B[a]P in terms of chromosomal aberration and micronucleus formation. DNA strand break levels in only B[a]P treated group remained significantly high from the control values (P < 0.001). The pretreatment of soy isoflavone showed gradual reduction in strand breaks significantly (P < 0.001) and dose dependently. Soy isoflavone pretreatment also decreased cytochrome P450 (CYP) content. The activity of CYP was also decreased dose dependently by pretreatment with soy isoflavone. The chemopreventive effect of soy isoflavone on the inhibition of CYP activity and DNA integrity mediate the possible mechanism of inhibition of genotoxicity.     

Benzo(a)pyrene induces oxidative stress,pro-inflammatory cytokines,expression of nuclear factor-kappa B and deregulation of wnt/beta-catenin signaling in colons of BALB/c mice

The incidence of colonic toxicity has been epidemiologically linked to the consumption of foods contaminated with benzo(a)pyrene (B[a]P). The present study investigated the effects of B[a]P on biomarkers of oxidative stress, inflammation and wnt-signaling in colon of BALB/c mice following exposure to 62.5, 125 and 250 mg/kg of B[a]P for 7 days by oral gavage. Exposure to B[a]P significantly decreased the colonic antioxidant enzymes activities and glutathione level with concomitant significant increase in myeloperoxidase activity, nitric oxide and lipid peroxidation levels. Colon histopathology results showed treatment-related lesions characterized by atrophy, mucosal ulceration and gland erosion in the B[a]P-treated mice. Immunohistochemistry analysis showed that B[a]P treatment increased the protein expression of nuclear factor kappa B, pro-inflammatory cytokines namely tumor necrosis factor alpha and interleukin-1β, as well as cyclooxygenase-2 and inducible nitric oxide synthase in the mice colon. Altered canonical wnt-signaling was confirmed by strong diaminobenzidine staining for p38 mitogen activated protein kinase, β-catenin expression and absence of adenomatous polyposis coli following B[a]P administration. The present data highlight that exposure to B[a]P induces colon injury via induction of oxidative and nitrosative stress, inflammatory biomarkers and dsyregulation wnt/β-catenin signaling, thus confirming the role of B[a]P in the pathogenesis of colonic toxicity.     

Ethanol Extract of Crataeva nurvala Stem Bark Reverses Cisplatin-induced Nephrotoxicity

Generation of free radicals in the kidney cortex plays an important role in the pathogenesis of cisplatin-induced dysfunction of renal proximal tubule cells. Previous studies carried out showed that an alcohol extract of Crataeva nurvala stem bark possessed antioxidant activity in rats, hence the present work aimed at evaluating the possible effect of the alcohol extract of C. nurvala on cisplatin-induced dysfunction model of renal proximal tubule cells by oxidative stress. The alcohol extract was administered orally for ten days at two dose levels of 250 and 500 mg/kg body weight, five days after administration of a single i.p. dose of cisplatin (5 mg/kg). Renal dysfunction was evaluated histologically by light microscopy and biochemically by measuring the concentrations of blood urea nitrogen, serum creatinine, lipid peroxidation, glutathione and catalase activity in the kidney cortex. The results suggest that the plant extract (250 and 500 mg/kg) was effective in significantly altering the indices of cisplatin induced dysfunction of renal proximal tubule cells under oxidative stress by decreasing the concentration of blood urea nitrogen, creatinine and lipid peroxidation. The increased glutathione and catalase activity are indicative of the antioxidant properties of C. nurvala stem bark extract.     

Tannic acid mitigates cisplatin-induced nephrotoxicity in mice

Cisplatin (CP) is a well-known chemotherapeutic drug that displays dose-limiting nephrotoxicity. In this study, tannic acid (TA), a naturally occurring plant polyphenol, was evaluated for its antioxidant and antigenotoxicity potential against the CP-induced renal oxidative stress and genotoxicity in Swiss albino mice. The mice were given a prophylactic treatment of TA orally at a dose of 40 and 80 mg/kg body weight (b wt) for 7 consecutive days before the administration of a single intraperitoneal (i.p.) injection of CP at 7 mg/kg b wt. The modulatory effects of TA on CP-induced nephrotoxicity and genotoxicity were investigated by assaying oxidative stress biomarkers, serum kidney toxicity markers, DNA fragmentation, alkaline unwinding, micronuclei assay, and by histopathological examination of kidney architecture. CP administration altered the antioxidant levels, enhanced lipid peroxidation, induced DNA strand breaks, and altered the levels of micronuclei among polychromatic erythrocytes (PCEs) significantly (p < 0.001). Pretreatment of TA in mice showed significant (p < 0.001) recovery in antioxidant status, viz., reduced glutathione content and its dependent enzymes, quinone reductase and γ-glutamyl transpeptidase. TA significantly (p < 0.001) reinstated the normal serum levels of blood urea nitrogen (BUN) and creatinine. TA showed strongly inhibited (p < 0.001) micronuclei induction, DNA strand breaks, and DNA fragmentation. Thus, TA as a phytochemical protects kidneys through its antigenotoxic activity and antioxidant potential.     

Anti-clastogenic effect of magnolol on benzo(a)pyrene-induced clastogenicity in mice.

It was previously reported that magnolol strongly inhibited the mutagenicity induced by the indirect mutagens [benzo(a)pyrene (B(a)P), 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 2-aminodipyrido[1,2-a:3',2'-d]imidazole (Glu-P-2), 2-aminoanthracene (2AA), and 7,12-dimethylbenz[a]anthracene (DMBA)] in Salmonella typhimurium TA98 and TA100 in the Ames test, and that the mechanism of this anti-mutagenic effect may involve the inhibition of the metabolic activation of indirect mutagen enzymes. In this study, the in vivo anti-clastogenic effect of magnolol against clastogenicity induced by B(a)P was evaluated using the micronucleus test in mice. Animals were treated with an oral administration of magnolol (1, 10, and 100 mg/kg) at -24, 0, 24, 48, 72, and 96 h before a single intraperitoneal injection of B(a)P. Peripheral blood specimens were prepared 48 h after administration of B(a)P, and analyzed by the acridine orange (AO) technique. The results indicated that magnolol inhibited clastogenicity induced by B(a)P at various administration times. In order to elucidate the mechanism behind this effect, we measured the activity of the detoxifying enzymes [UDP-glucuronosyltransferase (UGT) and glutathione-S-transferase (GST)] and antioxidative enzymes [superoxide dismutase (SOD) and catalase] in the liver when treated with an oral administration of magnolol at various administration times. Its effect on clastogenicity created by exposure to oxidative DNA damage-inducing X-ray irradiation was also evaluated using the micronucleus test in mice. Results showed that magnolol increased the activity of both UGT and SOD enzymes, and also inhibited the clastogenicity induced by X-ray irradiation. Magnolol had an anti-clastogenic effect on B(a)P in the micronucleus test as well as an anti-mutagenic effect on indirect mutagens in the Ames test. The anti-clastogenic effect of magnolol was also suggested by the increases in UGT and SOD enzyme activity, and by the attenuation of oxidative damage induced by X-ray irradiation.     

In vitro inhibition of carcinogen-induced mutagenicity by Cassia occidentalis and Emblica officinalis

Aqueous extracts of Cassia occidentalis Linn. (Leguminoceae) and Emblica officinalis Gaertn. (Euphorbiaceae) were screened for effectiveness in inhibiting mutagenicity of aflatoxin B1 (AFB1) and benzo[a]pyrene (B[a]P) in the Ames test. Antimutagenicity was evaluated using Salmonella typhimurium strains TA 98 and TA 100. In the assay, metabolic activation of AFB1 (0.5 microg/plate) and B[a]P (1 microg/plate) was mediated by rat liver S9 preparation. Although both plants inhibited mutagenicity, E. officinalis had more inhibitory effect than C. occidentalis. Their action is possibly mediated through interactions with microsomal activating enzymes. Their inhibitory action on chromosomal aberrations together with present results suggest that these plants have potent antimutagenic and anticarcinogenic activities against mutagens requiring metabolic activation.     

Ameliorative influence of Urtica dioica L against cisplatin-induced toxicity in mice bearing Ehrlich ascites carcinoma

Cisplatin (CP) is a widely used cytotoxic agent against cancer, and high doses of CP have been known to cause nephrotoxicity and hepatotoxicity. Some reports claim that antioxidants can reduce CP-induced toxicity. This study investigated the hepatoprotective, nephroprotective, and antioxidant activity of Urtica dioica L methanolic extract (UDME) against CP toxicity in Erhlich ascites tumor (EAT)-bearing mice. Levels of serum hepatic enzymes, renal function markers, and oxidant/antioxidant parameters of liver tissue were measured. Mice were inoculated with EAT on day 0 and treated with nothing else for 24 hours. After a single dose of CP administration on day 1, the extract was given at the doses of 50, 100, 200, and 400 mg/kg body weight daily during 6 days. Almost all doses of UDME performed a significant (P?相似文献   

Azadirachta indica attenuates cisplatin-induced neurotoxicity in rats

Objective:

The objective of this study is to investigate the neuroprotective effects of Azadirachta indica leaves against cisplatin (CP)-induced neurotoxicity.

Materials and Methods:

Female Wistar rats were treated with vehicle (control); a single intraperitoneal 5 mg/kg CP (CP group); neem leaves (orally 500 mg/kg) for 5 and 10 days, N5 and N10 groups, respectively; neem leaves (500 mg/kg) for 5 days after CP injection, collagenous protein nitrogen (CPN) group; neem leaves (500 mg/kg) for 5 days before CP injection, noncollagenous protein group and neem leaves in a dose of 500 mg/kg for 5 days before and after CP injection, noncollagenous protein nitrogen group. Rats were sacrificed 5 days after CP injection to determine neural lipid peroxidation (LPO), nitric oxide (NO), and glutathione (GSH) levels. The neuronal antioxidant enzymes were evaluated in brain homogenates.

Results:

CP injection increased LPO, NO levels and decreased GSH level, whereas neem reversed these effects. Morphological brain damage and apoptosis induction were apparent in the CP group. In the CPN group, the histological damage and apoptosis induction caused by CP was improved, whereas morphological findings of neem before and after CP injection implied a well preserved brain tissue. No changes, in biochemical parameters were observed with neem treated groups.

Conclusion:

This study suggests that methanolic extract of neem leaves may be of therapeutic benefit when used with CP.KEY WORDS: Azadirachta indica, cisplatin, neurotoxicity, apoptosis, rats     

Chemoprotective potential of Coccinia indica against cyclophosphamide-induced toxicity

Objective:

Although cyclophosphamide (CP), an alkylating agent, is used in the treatment of cancer owing to its broad-spectrum efficacy, its metabolites exhibit severe undesired toxicities in normal cells. The present study was aimed to investigate the chemoprotective potential of Coccinia indica against CP-induced oxidative stress, genotoxicity, and hepatotoxicity.

Materials and Methods:

Rodents were orally pre-treated with Coccinia indica extract (200, 400, and 600 mg/kg) for five consecutive days. On 5th day, these animals were injected with CP (50 mg/kg i.p) and sacrificed after 24 hrs. for the evaluation of oxidative stress, hepatotoxicity, micronucleus formation, and chromosomal aberrations.

Results:

We found that the CP significantly increased malondialdehyde (MDA) and decreased catalase and glutathione (GSH) levels in brain, and it was significantly reversed by Coccinia indica extract (400 and 600 mg/kg). Further, pre-treatment with Coccinia indica extract (200, 400, 600 mg/kg) significantly and dose-dependently reduced micronuclei formation and incidence of aberrant cells. We also found that the CP-induced increase in the serum biomarker enzymes like alkaline phosphatase (ALP), alkaline aminotransferase (ALT), and aspartate aminotransferase (AST) were significantly reduced by Coccinia indica extract.

Conclusion:

Thus, the present results indicate the protective effect of Coccinia indica extract against CP-induced oxidative stress, genotoxicity, as well as hepatotoxicity.KEY WORDS: Coccinia indica, cyclophosphamide, genotoxicity, oxidative stress     

Antidiabetic effect of Punica granatum flowers: Effect on hyperlipidemia,pancreatic cells lipid peroxidation and antioxidant enzymes in experimental diabetes

The present study investigated the effects of Punica granatum aqueous extract (PgAq) on streptozotocin (STZ) induced diabetic rats by measuring fasting blood glucose, lipid profiles (atherogenic index), lipid peroxidation (LPO) and activities of both non-enzymatic and enzymatic antioxidants. Diabetes was induced by single intraperitoneal injection of STZ (60 mg/kg) to albino Wistar rats. The increase in blood glucose level, total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), very low density lipoprotein (VLDL), LPO level with decrease in high density lipoprotein cholesterol (HDL-C), reduced glutathione (GSH) content and antioxidant enzymes namely, glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT) were the salient features observed in diabetic rats. On the other hand, oral administration of PgAq at doses of 250 mg/kg and 500 mg/kg for 21 days resulted in a significant reduction in fasting blood glucose, TC, TG, LDL-C, VLDL-C and tissue LPO levels coupled with elevation of HDL-C, GSH content and antioxidant enzymes in comparison with diabetic control group.     

Role of 5-HT(1B) receptors in the sensitization to amphetamine in mice.

The present study was designed to determine how 5-HT(1B) receptor ligands affected the development or the expression phase of sensitization to the amphetamine-induced locomotor response in mice. Mice were treated repeatedly (for 5 days) with amphetamine (2.5 mg/kg) in combination with either vehicle, N-[3-[3-(dimethylamino)ethoxy]-4-methoxyphenyl]-2'-methyl-4'-(5-methyl-1,2,4-oxadiazol-3-yl)-[1,1'-biphenyl]-4-carboxamide hydrochloride (SB 216641; an antagonist of 5-HT(1B) receptors), 3-(1,2,5,6-tetrahydro-4-pyridyl)-5-propoxypyrrolo[3,2-b]pyridine (CP 94,253; an agonist of 5-HT(1B) receptors), or SB 216641+CP 94,253; afterwards, on day 10, they received a challenge dose of amphetamine (2.5 mg/kg). In another experiment, mice were given either vehicle or amphetamine (2.5 mg/kg) for 5 days, and were then challenged with amphetamine (2.5 mg/kg) in combination with vehicle, SB 216641, or CP 94,253 on day 10. Locomotor hyperactivity induced by acute administration of amphetamine (day 1) was dose-dependently inhibited by SB 216641 and enhanced by CP 94,253, but not affected by a combination of SB 216641+CP 94,253. The 5-HT(1B) receptor ligands affected similarly the behavioral response to the challenge dose of amphetamine on day 10 (ca. 55-110% more potent than the response to its first administration) when they were combined with the psychostimulant during the development phase (days 1-5) of sensitization. On the other hand, neither SB 216641 nor CP 94,253 administered together with the challenge dose of amphetamine (day 10) affected its behavioral hyperactivity effect in mice treated repeatedly (days 1-5) with the psychostimulant alone. Our results suggest that 5-HT(1B) receptors may play a permissive role in the development, but not expression, of behavioral sensitization, as well as in the acute locomotor response to amphetamine in mice.     

Genotoxicity studies of stevia extract and steviol by the comet assay

The genotoxicity of steviol, a metabolite of stevia extract, was evaluated for its genotoxic potential using the comet assay. In an in vitro study, steviol at 62.5, 125, 250, and 500 micrograms/ml did not damage the nuclear DNA of TK6 and WTK1 cells in the presence and absence of S9 mix. In vivo studies of steviol were conducted by two independent organizations. Mice were sacrificed 3 and 24 hr after one oral administration of steviol at 250, 500, 1000, and 2000 mg/kg. DNA damage in multiple mouse organs was measured by the comet assay as modified by us. After oral treatment, stomach, colon, liver, kidney and testis DNA were not damaged. The in vivo genotoxicity of stevia extract was also evaluated for its genotoxic potential using the comet assay. Mice were sacrificed 3 and 24 hr after oral administration of stevia extract at 250, 500, 1000, and 2000 mg/kg. Stomach, colon and liver DNA were not damaged. As all studies showed negative responses, stevia extract and steviol are concluded to not have DNA-damaging activity in cultured cells and mouse organs.     

Phenolic extract of soybean (Glycine max) attenuates cisplatin-induced nephrotoxicity in rats

The present study investigated the modulatory role of phenolic extract of soybean (PESB) in a rat model of nephrotoxic acute renal failure induced by cisplatin. Cisplatin (2 mg/kg/day) was administered to the rats for 5 days and the animals were pretreated with PESB (250–1000 mg/kg). Blood urea nitrogen reduced by 49.8% and 59.0%, serum creatinine by 34.7% and 62.1% and urinary N-acetyl-β-d-glucosaminidase also decreased by 37.7% and 49.2% following treatment with 250- and 500-mg/kg doses of the extract respectively in the cisplatin-treated rats. The extract also significantly increased renal myeloperoxidase activity by 26.8% and 40.6% at these doses. PESB also decreased renal xanthine oxidase activity and serum nitrate/nitrite in the cisplatin-treated rats. In addition, PESB significantly attenuated the marked renal oxidative damage that accompanied cisplatin treatment. The extract improved liver histology and significantly increased the activities of the antioxidant enzymes measured [superoxide dismutase, catalase, glutathione-S-transferase], prevented glutathione depletion and decreased malondialdehyde level following cisplatin treatment. Furthermore, cisplatin-induced decrease in the activities of glucose-6-phosphatase and 5′-nucleotidase in these rats was attenuated only at 250 mg/kg dose of the extract. We concluded therefore that PESB via antioxidant and possibly anti-inflammatory actions offered protective benefit against cisplatin-mediated acute toxic injury to the kidney.     

Hypoglycaemic Potential of Mangifera indica Leaves in Rats

Hypoglycaemic activity of 50% ethanol extract of Mangifera indica tender leaves was studied in normal and streptozotocin induced diabetic rats. In normal rats, the extract was administered only once in doses of 100, 250 and 500 mg/kg per os. The highest decrease (37.73%) in plasma glucose levels was obtained with 250 mg dose after 8 h of administration. In diabetic rats, the extract produced significant antihyperglycaemic effect within 3 days when given at 250 mg/kg/day per os for 10 days. LD 50 of the extract was above 4.64 gm/kg per os.