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Objective: Gentamicin is an efficacious aminoglycoside antibiotic widely used to treat life-threatening Gram-negative bacteria infections. However, its specific non-targeted induction of nephrotoxicity is a worrying clinical challenge. The study explored the nephroprotective effect of Moringa oleifera seed oil (MOO) against gentamicin-induced oxidative nephrotoxicity, pro-inflammation, and apoptosis in male Wistar rats. Method: Twenty-four rats divided into 4 groups (n = 6) were administered MOO (5 ml/kg) for 16 days and/or gentamicin (100 mg/kg bw/d, ip) injected from day 11 to day 16. The renal antioxidant enzyme activities reduced glutathione, lipid peroxidation, and serum renal markers. Urea and creatinine levels were estimated. The renal expression of interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and nitric oxide (NO) were determined. Renal levels of inducible nitric oxide synthase (iNOS), nuclear factor-ĸB (NF-ĸB), and caspase-3 were determined to detect possible mechanism of inflammation and apoptosis with histology. Results: MOO prominently reduced serum creatinine and urea levels with amelioration of histopathological abrasions induced by gentamicin (GM). It significantly depressed oxidative stress through lowering of renal malondialdehyde (MDA) and elevation of renal superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities, and reduced glutathione (GSH) level. MOO restored renal content of IL-1β, IL-6, TNF-α, and NO, coupled with the mechanistic downregulation of NF-ĸB, iNOS, and caspase-3 activities. The histopathological alterations were ameliorated by MOO. Conclusions: MOO possesses marked nephroprotective effect against GM-induced renal damage via modulating oxidative stress, inflammation, and apoptosis in Wistar rats.

Background: Cadmium is an established carcinogen. Cadmium exposure resulted in skin carcinogenesis in rats. Furthermore, neurotransmitter-cancer interaction, tissue innervation, and angiogenesis influence cancer prognosis, metastasis, and survival. In this study, we evaluated the anticancer and neuro-protective potentials of MO 11 (isolated from Moringa oleífera leaves) and MS06 (isolated from Musa sapientum suckers) against in-vivo Cadmium Chloride (CdCI2)- induced skin toxicity. Methods: Twenty-four adult male wistar rats were randomly divided into six groups (n = 4). Group 1 was control. Groups 2-4 and 6 received a single intraperitoneal administration of 1.5 mg/kg CdCI2 on Day 1. Thereafter, Groups 3, 4, and 6 were post-treated with 15 mg/kg MO 11,15 mg/kg MO11 + 7 mg/kg MS06, and 3.35 mg/kg Doxorubicin respectively (Days 1-17). Group 5 received an olive oil dose (vehicle) (Days 1-17). Skin histopathology and tissue-enzyme-linked-immunosorbent assays (Tissue-ELISA) of neurotransmitters (Dopamine and Glutamate), biomarkers of myelination (Myelin Basic Protein), drug metabolism and carcinogenesis (Cytochrome-p450), apoptosis (Caspase-3 and p53), proliferation (Ki67), and angiogenesis (sVEGFR) were evaluated in skin homogenates. Data were statistically analyzed using the Mann-Whitney-U test at Z'<0.05. Results: Histopathological analyses revealed normal skin histology (Groups 3 and 4), mild skin histo-alterations (Group 6), and gross skin histopathological alterations (Group 2). Tissue-ELISA analyses showed upregulations of dopamine, Glutamate and Cytochrome-p450, but downregulations of Myelin Basic Protein, Caspase-3, KÍ67, p53, and sVEGFR in groups 3, 4, and 6, compared with group 2. MO 11 and MS06 achieved better anticancer effects than doxorubicin. Conclusion: Overall, MO 11 and MS06 possess histo-protective, neuro-protective, re-myelination, anti-proliferation, anti-angiogenesis, and anti-cancer potentials. [ABSTRACT FROM AUTHOR]

Background: Cadmium (Cd) is an established carcinogen. Cd-induced renotoxicity resulted in oxidative stress, loss of excretory kidney functions, and apoptosis of murine kidney cells. Objectives: This study evaluated renoprotective potentials of MO11 (isolated from Moringa oleifera leaves) and MS06 (isolated from Musa sapientum suckers) against Cd chloride (CdCl2)-induced renotoxicity, renal hyperplasia, and apoptosis in rats. Materials and Methods: Twenty-four adult male Wistar rats (average weight of 155 g) were randomly divided into seven groups (n = 4). Group 1 received physiological saline. Groups 2-4 and 6 received single intraperitoneal (i.p) administration of 1.5 mg/kg body weight of CdCl2 (i.p) (Day 1). Groups 3-4 and 6 were posttreated with 15 mg/kg body weight of MO11, 15 mg/kg body weight of MO11 +7 mg/kg body weight of MS06, and 3.35 mg/kg body weight of doxorubicin, respectively (days: 1-17). Group 5 received only olive oil dose (vehicle), respectively (days: 1-17). Kidney histopathology (hematoxylin and eosin technique) and enzyme-linked immunosorbent assay concentrations of biomarkers of proliferation (Ki67) and apoptosis (p53) in kidney homogenates of rats of Groups 1-6 were evaluated. Results: Histopathological analyses showed normal kidney histology in the rats of Groups 1-6. Posttreatments of CdCl2 -induced renotoxicity with MO11, MO11+MS06, and doxorubicin resulted in downregulations of Ki67 and p53 in Groups 3, 4, and 6 as compared with Group 2. Conclusion: MO11 and MS06 possess renoprotective, anti-proliferation, and anti-apoptosis potentials. [ABSTRACT FROM AUTHOR]

Objective: Gentamicin is an efficacious aminoglycoside antibiotic widely used to treat life-threatening Gram-negative bacteria infections. However, its specific non-targeted induction of nephrotoxicity is a worrying clinical challenge. The study explored the nephroprotective effect of Moringa oleifera seed oil (MOO) against gentamicin-induced oxidative nephrotoxicity, pro-inflammation, and apoptosis in male Wistar rats.Method: Twenty-four rats divided into 4 groups (n = 6) were administered MOO (5 ml/kg) for 16 days and/or gentamicin (100 mg/kg bw/d, ip) injected from day 11 to day 16. The renal antioxidant enzyme activities reduced glutathione, lipid peroxidation, and serum renal markers. Urea and creatinine levels were estimated. The renal expression of interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and nitric oxide (NO) were determined. Renal levels of inducible nitric oxide synthase (iNOS), nuclear factor-ĸB (NF-ĸB), and caspase-3 were determined to detect possible mechanism of inflammation and apoptosis with histology.Results: MOO prominently reduced serum creatinine and urea levels with amelioration of histopathological abrasions induced by gentamicin (GM). It significantly depressed oxidative stress through lowering of renal malondialdehyde (MDA) and elevation of renal superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities, and reduced glutathione (GSH) level. MOO restored renal content of IL-1β, IL-6, TNF-α, and NO, coupled with the mechanistic downregulation of NF-ĸB, iNOS, and caspase-3 activities. The histopathological alterations were ameliorated by MOO.Conclusions: MOO possesses marked nephroprotective effect against GM-induced renal damage via modulating oxidative stress, inflammation, and apoptosis in Wistar rats. [ABSTRACT FROM AUTHOR]