Effect of soy oil, orange (&lt;em&gt;Citrus sinensis&lt;/em&gt;) peel oil and their blends on total phospholipid, lipid peroxidation, and antioxidant defense system in brain tissues of normo rats

Erukainure, Ochuko L.; Ajiboye, John A.; Davis, Frank F.; Obabire, K.; Okoro, Emeka E.; Adenekan, Sunday; Adegbola, Mosebolatan Victoria; Awogbemi, B. J.; Odjobo, B. O.; Zaruwa, Moses Z.

doi:10.3989/gya.0373151

Cited by 2 publications

(2 citation statements)

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“…An increase in the levels of antioxidant enzymes has also been found in rats treated with CSPE in their diet. Erukainure et al (31) examined rats fed a diet consisting of 35% CSPE for 6 weeks. A significant increase in the levels of SOD and glutathione was observed following 6 weeks of treatment (31).…”

Section: Discussionmentioning

confidence: 99%

“…Erukainure et al (31) examined rats fed a diet consisting of 35% CSPE for 6 weeks. A significant increase in the levels of SOD and glutathione was observed following 6 weeks of treatment (31). In another study, in Wistar rats treated orally with a combination of Citrus aurantifolia and Cinnamomum burmannii at 100, 300 and 500 mg/kg, exhibited an increase in the levels of SOD following treatment (32).…”

Section: Discussionmentioning

confidence: 99%

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Integrated molecular docking, dynamic simulations and in vivo analysis of ethanol extract Citrus sinensis peel as an antioxidant and neurotrophic agent for ameliorating motor and cognitive functions in traumatic brain injury

Santoso,

Putra,

Syaban

et al. 2023

World Acad Sci J

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Traumatic brain injury (TBI) is the primary injury to the brain caused by mechanical forces. It is one of the leading causes of mortality in mid-life. Increased levels of inflammation and oxidation, and decreased levels of neurotrophic factor lead to a worsening of the condition. In previous studies, the authors demonstrated that the ethanol extract of Citrus sinensis peel (CSPE) functioned as an antioxidant using molecular docking and dynamic simulations. In the present study, in order to confirm these findings, a Marmarou weight drop model which included rats with TBI. Molecular docking against c-Jun N-terminal kinase 3 (JNK3) was also performed. The rats were divided into the sham-operated, control and treatment groups. The treatment groups received CSPE at 50, 250 and 500 mg/kg body weight (groups 1, 2 and 3, respectively) orally once a day for 7 days following the induction of TBI. Superoxide dismutase (SOD)1, SOD2, and brain-derived neurotrophic factor (BDNF) expression levels were analyzed using immunohistochemistry. Surviving neurons were analyzed using hematoxylin and eosin staining. Barnes' maze and wire grip tests were performed on the 1st, 3rd and 7th days following TBI. The results revealed a significant increase in the numbers of surviving neurons and in BDNF expression in groups 2 and 3, a higher expression of SOD1 in group 3, and a higher expression of SOD2 in all the treatment groups. Wire grip duration was significantly longer on the 7th day following TBI in group 3, and Barnes maze latency was significantly shorter on the 3rd and 7th days following TBI compared to the previous time in all treatment groups. Molecular docking analysis also revealed that CSPE compounds, particularly chanoclavine and nootkatone, interacted with JNK3 in the same binding pocket. On the whole, the present study demonstrates that CSPE helps protect the brain from damage by functioning as an antioxidant, increasing neurotrophic activities and inhibiting apoptosis. This reduces the overall neurological issues that are associated with TBI. However, further studies on the efficacy and safety of CSPE are required in order to determine its full potential in improving motor and cognitive functions following TBI.

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Section: Discussionmentioning

confidence: 99%