Camel milk rescues neurotoxic impairments induced by fenpropathrin via regulating oxidative stress, apoptotic, and inflammatory events in the brain of rats

Abd‐Elhakim, Yasmina M.; El-Sharkawy, Nabela I.; Mohammed, Hesham H.; Ebraheim, Lamiaa L.M.; Shalaby, Mohamed A.

doi:10.1016/j.fct.2019.111055

Cited by 41 publications

(27 citation statements)

References 83 publications

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“…The dose of cyclosporine and the experimental regimen was based on former studies that demonstrated the marked cyclosporine nephrotoxicity and robust renal inflammation [ 1 , 2 , 19 , 20 ]. Camel milk dose is consistent with former studies that demonstrated the 10 mL/kg dose as an effective dose against several models of inflammation in rats [ 10 , 13 , 14 , 15 , 16 ]. Likewise, the dose of quercetin has been reported as an effective dose against renal inflammation [ 21 ].…”

Section: Methodssupporting

confidence: 90%

“…Notably, camel milk has demonstrated unique features beyond its nutritive impact, compared to cow milk. In this regard, camel milk is low in lactose, cholesterol, and β-lactoglobulin/β-casein [ 15 ]. Moreover, it possesses a unique insulin-like activity which saves 30–35% of insulin dose in patients with diabetes mellitus [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, it possesses a unique insulin-like activity which saves 30–35% of insulin dose in patients with diabetes mellitus [ 16 ]. Furthermore, the rich content of lactoperoxidase and nanoantibodies has advocated its immune-modulatory, antibacterial, and antiviral features [ 15 ]. Compared to the milk of other species, including buffalo, cow, goat, sheep, and mare, camel milk is the richest in terms of the bioactive lactoferrin (220 mg/L), which imparts distinctive anti-inflammatory/antioxidant effects [ 17 , 18 ].…”

Section: Introductionmentioning

confidence: 99%

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Camel Milk Mitigates Cyclosporine-Induced Renal Damage in Rats: Targeting p38/ERK/JNK MAPKs, NF-κB, and Matrix Metalloproteinases

Arab

Ashour

Alqarni

et al. 2021

Biology

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Renal damage is a devastating adverse effect for cyclosporine; a widely used immunosuppressant drug. The present work examined the potential of camel milk, a natural agent with marked anti-inflammatory/antioxidant properties, to attenuate cyclosporine-induced renal injury. The kidney tissue was examined with the aid of Western blotting, immunohistochemistry, biochemical assays, including colorimetric and ELISA kits. The present findings revealed that camel milk (10 mL/kg/day; for 3 weeks by gavage) significantly lowered serum creatinine, BUN, and KIM-1 renal dysfunction markers. Mechanistically, camel milk inhibited renal inflammation, as seen by significant decrease of the pro-inflammatory cytokines (MCP-1, TNF-α, IL-1β, and IL-18) and extracellular degradation signals (MMP-2 and MMP-9) and enhanced the generation of the anti-inflammatory IL-10. Moreover, it inhibited the upstream pro-inflammatory p38/ERK/JNK MAPK pathway by lowering the phosphorylation of the 3 subfamilies of MAPKs (p38 MAPK, JNK1/2, and ERK1/2). Furthermore, camel milk curbed the NF-κB pathway activation by downregulating the protein expression of activated NF-κBp65, p-NF-κBp65, and p-IκBα proteins. Additionally, camel milk inhibited renal oxidative stress by lowering the MPO activity and augmenting the reduced/oxidized glutathione ratio and total antioxidant capacity. These findings propose that camel milk may be a promising agent that inhibits cyclosporine-triggered renal inflammation via curtailing the p38/ERK/JNK MAPK and NF-κB pathways, matrix metalloproteinases, and pro-inflammatory cytokines.

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Section: Methodssupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Camel Milk Mitigates Cyclosporine-Induced Renal Damage in Rats: Targeting p38/ERK/JNK MAPKs, NF-κB, and Matrix Metalloproteinases

Arab

Ashour

Alqarni

et al. 2021

Biology

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“…Ample evidence has demonstrated that several antioxidant agents have exerted beneficial ameliorative effects against CsA‐evoked nephrotoxicity, with the advantage of incurring minimal adverse effects (Wu et al., 2018). Camel milk (CM) is unique milk in terms of its high content of antioxidants, including the potent antioxidant lactoferrin, alongside several antioxidant trace elements and vitamins (Abd‐Elhakim et al., 2020; Ayoub et al., 2018). Evolving evidence has confirmed the marked antioxidant features of CM in several experimental models, where it augments the glutathione peroxidase (GPx), reduced glutathione (GSH), superoxide dismutase (SOD), and total antioxidant capacity (Arab et al, 2018a,b).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of oxidative stress and apoptosis by camel milk mitigates cyclosporine‐induced nephrotoxicity: Targeting Nrf2/HO‐1 and AKT/eNOS/NO pathways

Arab

Eid

Gad

et al. 2021

Food Science & Nutrition

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Cyclosporine (CsA) is a widely used immunosuppressive agent that incurs marked nephrotoxicity in the clinical setting. Thus, there is a need for finding safe/effective agents that can attenuate CsA‐induced kidney injury. Meanwhile, the underlying mechanisms for CsA‐associated nephrotoxicity are inadequately investigated, in particular, the AKT/eNOS/NO pathway. Here, the present work aimed to explore the potential of camel milk, a natural product with distinguished antioxidant/anti‐inflammatory actions, to ameliorate CsA‐induced nephrotoxicity in rats. The molecular mechanisms related to renal oxidative aberrations and apoptosis were studied, including Nrf2/HO‐1 and AKT/eNOS/NO pathways. The kidney tissues were inspected using histopathology, ELISA, Western blotting, and immunohistochemistry. The present findings demonstrated that camel milk (10 ml/kg) significantly lowered creatine, BUN, and NGAL nephrotoxicity markers and the aberrant histopathology, with similar efficacy to the reference quercetin. Moreover, camel milk suppressed the renal oxidative stress, as evidenced by significantly lowering NOX‐1 and lipid peroxides and significantly augmenting the renal antioxidant moieties (GSH, GPx, and SOD), thereby, driving the restoration of Nrf2/HO‐1 pathway. Meanwhile, camel milk counteracted the pro‐apoptotic reactions by significantly lowering Bax protein expression, caspase‐3 activity/cleavage, and PARP cleavage, alongside significantly increasing the expression of the proliferation signal PCNA. Regarding the anti‐apoptotic AKT/eNOS/NO pathway, camel milk activated its signaling by significantly increasing the protein expression of PI3Kp110, p‐AKT(Ser473)/total AKT, and p‐eNOS (Ser1177)/total eNOS besides significantly boosting the renoprotective NO levels. In conclusion, these findings reveal that camel milk may be a promising candidate for the alleviation of CsA‐induced nephrotoxicity.

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“…There have been studies published to indicate that other pesticide classes besides OPs and NMCs, such as pyrethroids and azoles, can also inhibit AChE in erythrocytes and/or the CNS (Abd‐Elhakim et al., 2020; Ansari et al., 2012; El‐Demerdash, 2007; Kale et al., 1999; Ncir et al., 2018; Noshy et al., 2018; Yousef et al., 2006). Instead of direct inhibition of AChE, these other pesticide classes are reported to induce oxidative stress, which might contribute to AChE inactivation in erythrocytes.…”

Section: Resultsmentioning

confidence: 99%

Cumulative dietary risk assessment of chronic acetylcholinesterase inhibition by residues of pesticides

Anastassiadou¹,

Choi²,

Čoja³

et al. 2021

EFS2

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A retrospective cumulative risk assessment of dietary exposure to pesticide residues was conducted for chronic inhibition of acetylcholinesterase. The pesticides considered in this assessment were identified and characterised in a previous scientific report on the establishment of cumulative assessment groups of pesticides for their effects on the nervous system. The exposure assessments used monitoring data collected by Member States under their official pesticide monitoring programmes in 2016, 2017 and 2018, and individual food consumption data from 10 populations of consumers from different countries and from different age groups. Exposure estimates were obtained by means of a two-dimensional probabilistic model, which was implemented in SAS ® software. The characterisation of cumulative risk was supported by an uncertainty analysis based on expert knowledge elicitation. For each of the 10 populations, it is concluded with varying degrees of certainty that cumulative exposure to pesticides contributing to the chronic inhibition of acetylcholinesterase does not exceed the threshold for regulatory consideration established by risk managers.

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Camel milk rescues neurotoxic impairments induced by fenpropathrin via regulating oxidative stress, apoptotic, and inflammatory events in the brain of rats

Cited by 41 publications

References 83 publications

Camel Milk Mitigates Cyclosporine-Induced Renal Damage in Rats: Targeting p38/ERK/JNK MAPKs, NF-κB, and Matrix Metalloproteinases

Camel Milk Mitigates Cyclosporine-Induced Renal Damage in Rats: Targeting p38/ERK/JNK MAPKs, NF-κB, and Matrix Metalloproteinases

Inhibition of oxidative stress and apoptosis by camel milk mitigates cyclosporine‐induced nephrotoxicity: Targeting Nrf2/HO‐1 and AKT/eNOS/NO pathways

Cumulative dietary risk assessment of chronic acetylcholinesterase inhibition by residues of pesticides

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