Bougainvillea spectabilis flowers extract protects against the rotenone-induced toxicity

Abdel-Salam, Omar M.E.; Youness, Eman R.; Ahmed, N.A.; El‐Toumy, Sayed A.; Souleman, Ahmed M. A.; Shaffie, Nermeen; Abouelfadl, Dalia M.

doi:10.1016/j.apjtm.2017.05.013

Cited by 18 publications

(20 citation statements)

References 42 publications

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“…Our data also show that rotenone can result in significant inhibition of BChE activity in the brain tissues which is in agreement with previous observations [54]. Rotenone was also demonstrated…”

Section: Rossupporting

confidence: 93%

“…Excessive nitric oxide can result in inhibition of mitochondrial respiration, and cellular energy depletion [52,53]. Rotenone also induces a state of neuroinflammation in the brain tissue [47,54]. This toxicant has been shown to increase the expression of tumor necrosis factor-alpha (TNF-α) as well as the level of monocyte chemoattractant protein-1 (MCP-1) [47] and interleukin-1β [54] in the rat brain.…”

Section: Discussionmentioning

confidence: 99%

“…Rotenone also induces a state of neuroinflammation in the brain tissue [47,54]. This toxicant has been shown to increase the expression of tumor necrosis factor-alpha (TNF-α) as well as the level of monocyte chemoattractant protein-1 (MCP-1) [47] and interleukin-1β [54] in the rat brain. Rotenone thus causes the development of oxidative stress and neuroinflammation, two fundamental pathologic processes encountered in the brain of human Parkinson's disease [9,16,17].…”

Section: Discussionmentioning

confidence: 99%

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Neuroprotection by Montelukast against Rotenone-Induced Rat Brain Damage

Abdel-Salam

Medhat

Sleem

et al. 2018

ROS

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| Montelukast is a cysteinyl-leukotriene receptor antagonist used in asthma prophylaxis. In this study, the effect of montelukast (10 or 20 mg/kg) on neuronal damage and oxidative stress induced in the rat brain by rotenone was examined. Rats were treated with rotenone subcutaneously at 1.5 mg/kg every other day alone or along with montelukast. The control group received the vehicle dimethyl sulfoxide (DMSO). The results showed that compared with the vehicle-treated group, rotenone resulted in increased brain lipid peroxidation by 84.5% as assessed by malondialdehyde (MDA) content. Nitric oxide increased by 77.4% while reduced glutathione (GSH) and total antioxidant capacity (TAC) decreased by 37.7% and 68.6%, respectively. In addition, the activities of superoxide dismutase (SOD), paraoxonase-1 (PON-1), and butyrylcholinesterase (BChE) significantly decreased by 34.6%, 68%, and 75.2%, respectively, after rotenone injection. Rotenone caused neurodegenerative changes in the cerebral cortex and substantia nigra. The administration of montelukast along with rotenone decreased MDA by 34.1-53.6%, nitric oxide by 51.6-64.7%, increased GSH content by 20.7-65.8%, and increased TAC by 109.6-156.2%. SOD activity increased by 50-62.5%, PON-1 activity by 161.1-203.7%, and BChE activity by 135.3-274.3% compared with respective rotenone control values. The rotenone-induced neuronal damage was ameliorated dose-dependently by montelukast. These results indicate that montelukast exerts a neuroprotective effect in the rotenone model of neurotoxicity. The neuroprotective action of montelukast is likely to involve an inhibitory effect on oxidative stress and nitric oxide. It is suggested that montelukast could be of value in the adjunctive treatment of Parkinson's disease.

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Section: Rossupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Neuroprotection by Montelukast against Rotenone-Induced Rat Brain Damage

Abdel-Salam

Medhat

Sleem

et al. 2018

ROS

Self Cite

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“…In order to induce PD in rats, rotenone (ROT, Sigma-Aldrich, Poznań, Poland) was injected subcutaneously once daily for 35 days in a dose of 1.3 mg/kg body weight. The doses and schedule of ROT used in the present study were established based on our results from preliminary studies, and they are similar to those previously described in published reports [33,39,57,65] with slight modifications (Figure 10). Forty rats (cohort #1) were divided randomly into four groups, with 10 animals in each.…”

Section: Experimental Designmentioning

confidence: 75%

Neuroprotective Effects of Pomegranate Juice against Parkinson’s Disease and Presence of Ellagitannins-Derived Metabolite—Urolithin A—In the Brain

Kujawska

Jourdes

Kurpik

et al. 2019

IJMS

109

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Pomegranate juice is a rich source of ellagitannins (ETs) believed to contribute to a wide range of pomegranate’s health benefits. While a lot of experimental studies have been devoted to Alzheimer disease and hypoxic-ischemic brain injury, our knowledge of pomegranate’s effects against Parkinson’s disease (PD) is very limited. It is suggested that its neuroprotective effects are mediated by ETs-derived metabolites—urolithins. In this study, we examined the capability of pomegranate juice for protection against PD in a rat model of parkinsonism induced by rotenone. To evaluate its efficiency, assessment of postural instability, visualization of neurodegeneration, determination of oxidative damage to lipids and α-synuclein level, as well as markers of antioxidant defense status, inflammation, and apoptosis, were performed in the midbrain. We also check the presence of plausible active pomegranate ETs-derived metabolite, urolithin A, in the plasma and brain. Our results indicated that pomegranate juice treatment provided neuroprotection as evidenced by the postural stability improvement, enhancement of neuronal survival, its protection against oxidative damage and α-synuclein aggregation, the increase in mitochondrial aldehyde dehydrogenase activity, and maintenance of antiapoptotic Bcl-xL protein at the control level. In addition, we have provided evidence for the distribution of urolithin A to the brain.

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“…Both extracts caused further inhibition of PON-1 activity while the yellow extract resulted in further inhibition of BChE activity. Histopathological studies indicated that both extracts protected against brain, liver, and kidney damage caused by the toxicant [ 52 ].…”

Section: Pharmacological Activitymentioning

confidence: 99%

Bougainvillea Genus: A Review on Phytochemistry, Pharmacology, and Toxicology

Abarca-Vargas

Petricevich

2018

Evidence-Based Complementary and Alternative Medicine

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This review discusses the current knowledge of the phytochemistry and in vitro and in vivo evaluations carried out using the extracts and, where appropriate, the main active components isolated from the genus Bougainvillea. Out of 18 species, most phytochemical, pharmacological, and toxicological studies focused on four species with different cultivars and one hybrid. Some plants are used for the treatment of various health disorders. Numerous phytochemical investigations of plants in this genus confirm the presence of aliphatic hydrocarbons, fatty acids, fatty alcohols, volatile compounds, phenolic compounds, peltogynoids, flavonoids, phytosterols, terpenes, carbohydrates, and betalains. Various studies have confirmed that these extracts or active substances that were isolated from the genus Bougainvillea have multiple pharmacological activities. Some species of Bougainvillea have emerged as sources of traditional medicine in human health. More studies of the phytochemical, pharmacological, and toxicological properties and their mechanisms of action, safety, and efficacy in all Bougainvillea species, cultivars, and hybrids are advisable for future research.

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Bougainvillea spectabilis flowers extract protects against the rotenone-induced toxicity

Cited by 18 publications

References 42 publications

Neuroprotection by Montelukast against Rotenone-Induced Rat Brain Damage

Neuroprotection by Montelukast against Rotenone-Induced Rat Brain Damage

Neuroprotective Effects of Pomegranate Juice against Parkinson’s Disease and Presence of Ellagitannins-Derived Metabolite—Urolithin A—In the Brain

Bougainvillea Genus: A Review on Phytochemistry, Pharmacology, and Toxicology

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