scholarly journals Anti-apoptotic effects of 2-pyrrolidone derivatives in cerebral ischemia

2021 ◽  
Vol 9 (4) ◽  
pp. 517-526
Author(s):  
Dmitriy I. Pozdnyakov ◽  
◽  
Anastasiya V. Sosnovskaya ◽  
Andrey V. Mamleyev ◽  
Alina A. Ladyka ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Caspase 3 ◽  
Reference Drug ◽  
Brain Necrosis ◽  
Wide Range ◽  
Ischemic Period ◽  
Apoptotic Effects ◽  
The Brain ◽  
Ischemic Events ◽  
Neuroprotective Action

INTRODUCTION: Uncontrolled course of apoptosis reactions underlies a wide range of pathological processes, including ischemic events. AIM: To evaluate the anti-apoptotic properties of some racetams in experimental brain ischemia in rats. MATERIALS AND METHODS: Cerebral ischemia was modeled in Wistar rats by irreversible occlusion of the middle cerebral artery. The test-compounds and the reference drug piracetam were administered per os at a dose of 250 mg/kg. After 72 hours of the ischemic period, the activity of apoptotic systems in the brain tissue was evaluated by determining the concentration of the apoptotic-inducing factor (AIF), caspase-3, ionized calcium, the latent opening time of the mitochondrial transition permeability pore and the zone of brain necrosis. RESULTS: The study showed that the use of the studied compounds contributed to a decrease in the intensity of reactions, both caspase-dependent and caspase-independent apoptosis, which was reflected in a decrease in the concentration of AIF and caspase-3 by 32.4% (p < 0.05); 34.6% (p < 0.05); 31.1% (p < 0.05), and 41.9% (p < 0.05); 39.1% (p < 0.05); 34.5% (p < 0.05) when PirPr, PirAc and PirBut were administered, respectively. Also, the use of the studied substances led to an increase in the latent period of opening the mitochondrial transition permeability pore, a decrease in the concentration of intracellular calcium and the zone of brain necrosis. At the same time, the pharmacological effect of the administration of the compound PirAc exceeded the effect of piracetam and other test substances. CONCLUSIONS: Based on the results obtained, it can be assumed that the studied racetams have neuroprotective action, realized through suppression of the reactions of apoptosis.

scholarly journals Characteristics of nervous tissue after modeling of focal cerebral ischemia in rats at different periods of reperfusion

2018 ◽  
Vol 24 (3) ◽  
pp. 58-64
Author(s):  
O.I. Savchuk ◽  
G.G. Skibo
Keyword(s):  
Cerebral Ischemia ◽  
Brain Damage ◽  
Nervous Tissue ◽  
Focal Cerebral Ischemia ◽  
Tactile Sensitivity ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Ischemic Period ◽  
The Brain ◽  
Occlusion Period

The stroke-causing problems are extremely important in Ukraine. This makes a heavy burden not only on the health care system, but also on the whole society as a whole. That's why we've studied structural and ultrastructural changes of cortical neurons and striatum of the brain and the development of delayed death of nerve cells after the modeling of the middle cerebral artery occlusion (MCAO) and post ischemic period in rats. We've analyzed the data at different terms after modeling of MCAO. The purpose of the study was to investigate the changes in the nervous tissue in the modeling of focal cerebral ischemia by monofilament occlusion of MCAO in rats at different periods of reperfusion. The statistical processing of primary digital experimental data was carried out using the software Statistica 6.0. It was confirmed that the 60-minute occlusion of the MCAO is an adequate model of focal ischemic brain damage in rats. Changes of locomotor activity and a tactile sensitivity were determined in rats after occlusion and after reperfusion during the post-period period. It was found that in the experimental group with a reperfusion period of 72 hours, a clear increase of the volume of the ischemic area of the brain, accompanied by significant neurological deficiency, was observed. Reduced research activity of the rats was revealed, which was shown in the decrease of the number of squares they crossed, the number of racks, the increase of acts of grooming and the duration of acts of frizings. Following ischemic brain damage, there was also a disbalance of somato-sensory functions, as evidenced by an increase in the time during which the animal took a test stimulus ("Sticky tape") from both the anterior paws when tested for tactile sensitivity (adhesive removal test). An electron microscopic study of the cortex showed that dark wrinkled neurons and enlightened swollen neurons were observed at 72 hours of post-occlusion period, indicating different ways of death of these cells. Changes in striatum were similar to changes in the cortex, which progressed with an increase in the post-occlusion period. The protocol of the serial evaluation of neurological disorders used after MCAO modeling allowed detecting long-term stable functional disorders in laboratory rats. The obtained data indicate significant changes in the structure of the cortex and striatum in the post-ischemic period and the progressive nature of these changes.

Acute Silent Cerebral Ischemia Occurs More Frequently Than Silent Cerebral Infarction In Children with Sickle Cell Anemia

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 268-268 ◽  
Author(s):  
Charles T. Quinn ◽  
Robert C. McKinstry ◽  
Michael M. Dowling ◽  
William S. Ball ◽  
Michael A. Kraut ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Sickle Cell ◽  
Brain Mri ◽  
Incidence Rates ◽  
Restricted Diffusion ◽  
Sensory Deficits ◽  
Acute Cerebral Ischemia ◽  
T2 Hyperintensity ◽  
The Brain ◽  
Ischemic Events

Abstract Abstract 268 Background: Children with sickle cell anemia (HbSS) are at high risk of overt stroke and clinically silent cerebral infarction (SCI). SCI is an infarct-like lesion visualized on magnetic resonance imaging (MRI) of the brain that produces no corresponding motor or sensory deficits. The prevalence of SCI in HbSS is approximately 20 – 30% by 16 years of age, but less is known about its incidence. The Cooperative Study of Sickle Cell Disease (CSSCD) found the incidence of new or more extensive SCI in children with HbSS to be 7 events per 100 patient-years. Given that SCI is clinically silent, the only way to determine its incidence (the number of new events occurring in a specific time-period) is to screen with two sequential MRIs of the brain. MRI can also detect acute cerebral ischemia in asymptomatic patients using diffusion-weighted imaging (DWI). The incidence of acute silent cerebral ischemic events (ASCIEs) is not known. A clinical trial setting provides a unique opportunity to determine the incidence of ASCIEs and SCI in children with HbSS. Objectives: To determine the incidence rates of (1) ASCIEs in children with HbSS without prior evidence of focal neurological deficits and (2) new, recurrent SCI in children with HbSS who have pre-existing SCI. Methods: We studied a cohort of children with HbSS and sickle-β0-thalassemia who had brain MRIs for the Silent Infarct Transfusion Trial. All participants had no prior history of overt stroke, seizures, or transient ischemic attacks. ASCIE was defined as an infarct-like lesion on brain MRI without corresponding motor or sensory deficits that appeared as a focus of T2 hyperintensity with restricted diffusion on DWI sequences. SCI was defined an infarct-like lesion without corresponding motor or sensory deficits that appeared as a focus of T2 hyperintensity without restricted diffusion. Given that acute cerebral ischemia appears as a focus of restricted diffusion on DWI for 10 days, we assumed that each MRI scan provided 10 patient-days of observation for detecting ASCIE. Therefore, the incidence of ASCIEs was calculated using a single MRI per patient. The incidence of new or more extensive SCI in children with pre-existing SCI was determined in those who had two MRIs each (screening and pre-randomization). We statistically compared the incidence rates of ASCIEs and SCI obtained by these two different methods. For all ASCIEs and new SCI events, a medical history tool was completed at the local site at the time of MRI of the brain. Results: In total, 972 MRIs were studied (745 screening, 227 pre-randomization). There were 844 MRIs with DWI sequences, providing 23.1 patient-years of observation in 640 children (52% male; mean age 9.7 years). ASCIEs were detected on 1.2% (10 of 844 MRIs), corresponding to an incidence of 43.3 (95% CI: 20.7 – 79.6) events per 100 patient-years. Nine of the 10 ASCIEs were detected incidentally; 1 ASCIE occurred in a participant who was recovering from a recent episode of acute chest syndrome (onset 5 days before MRI) complicated by severe anemia and hypertension. Standard neurological examination was normal in all cases. Two of the 10 participants with ASCIEs had follow-up MRIs of the brain 4 to 10 months later; one had SCI in the same location as the previously detected acute ischemia, but the other had no residual lesion in the same location. Thus, not all ASCIEs produce detectable SCI. A total of 220 participants (55% male; mean age 10.0 years) had both screening and pre-randomization MRIs. The mean interval between the two MRIs was 124.3 days (range: 14 – 645), providing 74.9 patient-years of observation. All screening MRIs showed baseline SCI. New, recurrent SCI was detected on pre-randomization MRI in 8 participants, corresponding to an incidence of 10.7 events per 100 patient-years (95% CI: 4.6 – 21.0). The incidence of ASCIEs was 4-fold higher than recurrent SCI (43.2 vs. 10.7 events per 100 patient-years; P=0.001). Conclusions: The incidence of recurrent SCI was similar to CSSCD findings. However, we show that children with HbSS experience acute cerebral ischemic events far more frequently than previously recognized. These acute ischemic events are mostly clinically silent, potentially reversible radiographically, and not associated with antecedent medical events. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Intravenous Administration of Coenzyme Q10 in Acute Period of Cerebral Ischemia Decreases Mortality by Reducing Brain Necrosis and Limiting Its Increase within 4 Days in Rat Stroke Model

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1240
Author(s):  
Obolenskaia Olga Nikolaevna ◽  
Gorodetskaya Evgeniya Aronovna ◽  
Kalenikova Elena Igorevna ◽  
Belousova Margarita Alekseevna ◽  
Gulyaev Mikhail Vladimirovich ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Intravenous Administration ◽  
Coenzyme Q10 ◽  
Brain Lesion ◽  
Neurological Status ◽  
Brain Necrosis ◽  
Rate Improvement ◽  
The Brain ◽  
Targeting Effect

Oxidative stress plays a key role in the pathogenesis of ischemic stroke. Coenzyme Q10 has a multi-targeting effect and may protect the brain against ischemic damage. The aim of our study was to evaluate the neuroprotective potential of ubiquinol by its intravenous administration. The study was performed on rats; a stroke was modeled by occlusion of the middle cerebral artery. On days 1 and 4 after ischemia, the neurological deficit and volume of the brain lesion were determined by MRI and TTC staining. Intravenous administration of coenzyme Q10 led to a decrease in rat mortality rate, improvement in neurological status, and decrease in the brain necrosis area in acute and delayed period after cerebral ischemia. A single intravenous administration of ubiquinol led to a limitation of the size of the brain damage for at least four days after ischemia. Thus, intravenous administration of coenzyme Q10 has a persistent neuroprotective potential. This finding suggests a possible therapeutic role of ubiquinol in acute ischemic conditions.

Angelica sinensis Exerts Angiogenic and Anti-apoptotic Effects Against Cerebral Ischemia–Reperfusion Injury by Activating p38MAPK/HIF-1α/VEGF-A Signaling in Rats

2017 ◽  
Vol 45 (08) ◽  
pp. 1683-1708 ◽  
Author(s):  
Chin-Yi Cheng ◽  
Tin-Yun Ho ◽  
Chien-Yun Hsiang ◽  
Nou-Ying Tang ◽  
Ching-Liang Hsieh ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Cytochrome C ◽  
Cerebral Infarction ◽  
P38 Mapk ◽  
Caspase 3 ◽  
Ischemia Reperfusion ◽  
Angelica Sinensis ◽  
Ischemic Penumbra ◽  
Study Results ◽  
Apoptotic Effects

This study evaluated the effects of Angelica sinensis extract [Dang Gui (DG)] administered before 60[Formula: see text]min of middle cerebral artery occlusion followed by 3[Formula: see text]d of reperfusion and investigated the involvement of mitogen-activated protein kinase (MAPK)/hypoxia-inducible factor (HIF)-1[Formula: see text] signaling in the cortical ischemic penumbra. DG was intraperitoneally administered at a dose of 0.25[Formula: see text]g/kg (DG-0.25g), 0.5[Formula: see text]g/kg (DG-0.5g), or 1[Formula: see text]g/kg (DG-1g) 30[Formula: see text]min before the onset of cerebral ischemia. Our study results revealed that DG-0.5g and DG-1g pretreatment effectively attenuated cerebral infarct and improved neurological deficits. DG-0.5g and DG-1g pretreatment significantly downregulated glial fibrillary acidic protein (GFAP), cytochrome c, and cleaved caspase-3 expression and upregulated phospho-p38 MAPK (p-p38 MAPK)/p38 MAPK, phospho-cAMP response element-binding protein (p-CREB)/CREB, cytosolic and mitochondrial phospho-Bad (p-Bad)/Bad ratios, and HIF-1[Formula: see text], vascular endothelial growth factor-A (VEGF-A), phospho-90 kDa ribosomal S6 kinase (p-p90RSK), and von Willebrand factor (vWF) expression in the cortical ischemic penumbra. Pretreatment with SB203580, a p38 MAPK inhibitor, dramatically abrogated the upregulating effects of DG-1g on p-p38 MAPK/p38 MAPK, p-CREB/CREB, and p-Bad/Bad ratios and HIF-1[Formula: see text], VEGF-A, and vWF expression and the downregulating effects of DG-1g on GFAP, cytochrome c, cleaved caspase-3, and cerebral infarction. DG-0.5g and DG-1g pretreatment provided neuroprotective effects against astrocyte-mediated cerebral infarction by activating angiogenic and anti-apoptotic signaling. Moreover, the angiogenic and anti-apoptotic effects of DG pretreatment can be attributed to the activation of p38 MAPK/HIF-1[Formula: see text]/VEGF-A/vWF signaling and p38 MAPK/HIF-1[Formula: see text]/VEGF-A/p-Bad-related regulation of cytochrome c/caspase-3 signaling, respectively, in the cortical ischemic penumbra 3[Formula: see text]d after reperfusion.

scholarly journals Сerebroprotective effect of some phenolic acids under conditions of experimental brain ischemia

2020 ◽  
Vol 7 (6) ◽  
pp. 332-339
Author(s):  
A. V. Voronkov ◽  
D. I. Pozdnyakov ◽  
S. A. Nigaryan
Keyword(s):  
Cerebral Ischemia ◽  
Gallic Acid ◽  
Phenolic Acids ◽  
Cerebral Edema ◽  
Focal Cerebral Ischemia ◽  
Lactate Concentration ◽  
Edema Formation ◽  
Reference Drug ◽  
Male Wistar Rats ◽  
The Brain

The aim of the study was to evaluate the cerebroprotective effect of some phenolic acids under the conditions of experimental cerebral ischemia in rats.Materials and methods. The experiment was conducted on male Wistar rats weighing 220–240 g. Focal cerebral ischemia was modeled by irreversible right-sided thermocoagulation of the middle cerebral artery under chloral hydrate anesthesia (350 mg/kg, intraperitoneally). The experimental compounds (4-hydroxy-3.5-di-tert-butyl cinnamic acid, caffeic acid and gallic acid 100 mg/kg each compound) and a reference drug (Mexicor – 100 mg/kg) were administered intragastrically next day after the surgery and then for three daysrunning. The effect of the test-compounds on the cognitive functions of the rats was evaluated by CRPA and TEA tests. The influence of the compounds on the changes in the concentration of lactate, pyruvate, homocysteine, as well as the degree of cerebral edema formation and necrosis of the brain tissue, were studied.Results. In the study, it has been established that against the background of the focal cerebral ischemia, the administration of caffeic, 4-hydroxy-3,5-di-tert-butylcinnamic and gallic acid, contributed to the preservation of a memorable trace in rats, as well as a decrease in lactate concentration (by 40.37% (p<0.05), 151.26% (p<0.05), 48.02% (p<0.05)) and pyruvate (by 96.6,% (p<0.05), 38, 78% (p<0.05), 33.3% (p<0.05)), homocysteine (by 59.6% (p<0.05), 102.18% (p<0.05), 28.8% (p<0.05)), аnecrosis zone (by 122.79% (p<0.05), 165.11% (p<0.05), 12.38% (p<0,05)) and cerebral edema (by 10.47% (p<0.05), 11.08% (p<0.05), 9.92% (p<0.05)) relative to the NC group of rats.Conclusion. The obtained data indicate the possibility of further detailed investigation of the cerebroprotective effect of 4-hydroxy-3,5-di-tert-butylcinnamic, caffeic and gallic acids.

Exploring the Role of Remote Ischemic Preconditioning In Long Term Cognitive Impairment after Global Ischemia-Reperfusion-Induced Vascular Dementia in Mice

2020 ◽  
Author(s):  
Amteshwar Singh Jaggi
Keyword(s):  
Cognitive Impairment ◽  
Cerebral Ischemia ◽  
Vascular Dementia ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Remote Ischemic Preconditioning ◽  
Global Cerebral Ischemia ◽  
Cerebral Ischemic ◽  
The Brain

Aim: The aim of the present study is to explore the neuroprotective effects of remote ischemic preconditioning in long term cognitive impairment after global cerebral ischemia induced-vascular dementia in mice. Material and methods: The mice were subjected to global cerebral ischemia by occluding the bilateral common carotid arteries for 12 minutes followed by the 24 hours of the reperfusion. The remote ischemic preconditioning stimulus was delivered in the form of 4 cycles of ischemia/reperfusion for 5 minutes each. The cerebral ischemic injury induced-long term cognitive impairment-related learning and memory alterations was assessed using morris water maze, the motor performances of the animals were evaluated using rota-rod test and neurological severity score. The cerebral infract size of the brain were quantified using triphenyltetrazolium chloride staining. Results: Global cerebral ischemia causes long term memory impairment, decreases motor performances and increases the brain infract size in animals. The delivery of remote ischemic preconditioning stimulus significantly abolished the long-term cognitive impairment and ameliorates the motor performances as well as cerebral infract size in brain. Conclusion: The remote ischemic preconditioning mediates neuro protection against global cerebral ischemic injury induced long-term cognitive impairment.

DNA Damage and Repair in the Brain After Cerebral Ischemia

2001 ◽  
Vol 1 (6) ◽  
pp. 483-495 ◽  
Author(s):  
Bentham Science Publisher Philip K. Liu
Keyword(s):  
Dna Damage ◽  
Cerebral Ischemia ◽  
Dna Damage And Repair ◽  
The Brain

Minocycline inhibits mTOR signaling activation and alleviates behavioral deficits in the Wistar rats with acute ischemia stroke

2020 ◽  
Vol 19 ◽  
Author(s):  
Shengyuan Wang ◽  
Chuanling Wang ◽  
Lihua Wang ◽  
Zhiyou Cai
Keyword(s):  
Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Mammalian Target Of Rapamycin ◽  
Mtor Signaling ◽  
Acute Ischemia ◽  
Intragastric Administration ◽  
Underlying Mechanisms ◽  
Signaling Activation ◽  
The Brain ◽  
Minocycline Therapy

Background: Mammalian target of rapamycin (mTOR) has been evidenced as a multimodal therapy in the path-ophysiological process of acute ischemic stroke (AIS). However, the pathway that minocycline targets mTOR signaling is not fully defined in the AIS pathogenesis. This study is to aim at the effects of minocycline on the mTOR signaling in the AIS process and further discover the underlying mechanisms of minocycline involved in the following change of mTOR signaling-autophagy. Methods: Cerebral ischemia/reperfusion (CIR) rat animal models were established with the transient suture occlusion into middle cerebral artery. Minocycline (50mg/kg) was given by intragastric administration. The Morris water maze was used to test the cognitive function of animals. Immunohistochemistry and immunofluorescence were introduced for testing the lev-els of synaptophysin and PSD-95. Western blot was conducted for investigating the levels of mTOR, p-mTOR (Ser2448), p70S6, p-p70S6 (Thr389), eEF2k, p-eEF2k (Ser366), p-eIF4B (Ser406), LC3, p62, synaptophysin and PSD-95. Results: Minocycline prevents cognitive decline of the MCAO stroke rats. Minocycline limits the expression of p-mTOR (Ser2448) and the downstream targets of mTOR [p70S6, p-p70S6 (Thr389), eEF2k, p-eEF2k (Ser366) and p-eIF4B (Ser406)] (P<0.01), while minocycline has no influence on mTOR. LC3-II abundance and the LC3-II/I ratio were upregu-lated in the hippocampus of the MCAO stroke rats by the minocycline therapy (P<0.01). p62 was downregulated in the hippocampus from the MCAO stroke rats administrated with minocycline therapy(P<0.01). The levels of SYP and PSD-95 were up-regulated in the brain of the MCAO stroke rats administrated with minocycline therapy. Conclusion: Minocycline prevents cognitive deficits via inhibiting mTOR signaling and enhancing autophagy process, and promoting the expression of pre-and postsynaptic proteins (synaptophysin and PSD-95) in the brain of the MCAO stroke rats. The potential neuroprotective role of minocycline in the process of cerebral ischemia may be related to mitigating is-chemia-induced synapse injury via inhibiting activation of mTOR signaling.

scholarly journals Apoptotic Effects of Xanthium strumarium via PI3K/AKT/mTOR Pathway in Hepatocellular Carcinoma

2019 ◽  
Vol 2019 ◽  
pp. 1-13
Author(s):  
Juyoung Kim ◽  
Kyung Hee Jung ◽  
Hyung Won Ryu ◽  
Doo-Young Kim ◽  
Sei-Ryang Oh ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Growth ◽  
Caspase 3 ◽  
Mtor Pathway ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Mechanistic Study ◽  
Migration And Invasion ◽  
Xanthium Strumarium ◽  
Apoptotic Effects ◽  
Hcc Cells

Xanthium strumarium (XS) has been traditionally used as a medicinal herb for treating inflammatory diseases, such as appendicitis, chronic bronchitis, rheumatism, and rhinitis. In this study, we yielded ethanol extracts from XS and investigated whether they could inhibit the progression of hepatocellular carcinoma (HCC) and its underlying mechanism. The XS-5 and XS-6 extracts dose-dependently inhibited the growth and proliferation in HCC cell lines. The apoptotic effects of them were observed via increased levels of cleaved caspase-3 and cleaved PARP, as well as elevated numbers of terminal deoxynucleotidyl transferase-mediated dUTP-biotin end labeling- (TUNEL-) positive apoptotic cells. They also decreased XIAP and Mcl-1 expression via loss of mitochondrial membrane potential. Additionally, they inhibited the invasion and migration of HCC cells. In an ex vivo model, the extracts significantly inhibited tumor cell growth and induced apoptosis by increasing the expression of the cleaved caspase-3. A mechanistic study revealed that they effectively suppressed PI3K/AKT/mTOR signaling pathways in HCC cells. Taken together, our findings demonstrate that they could efficiently not only induce apoptosis but also inhibit cell growth, migration, and invasion of human HCC cells by blocking the PI3K/AKT/mTOR pathway. We suggest XS-5 and XS-6 as novel natural anti-HCC agents.

Evaluation of antioxidant enzyme content, phenolic content, and antibacterial activity of Commiphora gileadensis grown in Saudi Arabia

2021 ◽  
Vol 19 (4) ◽  
pp. 329-343
Author(s):  
Yaaser Q. Almulaiky ◽  
Ammar AL-Farga
Keyword(s):  
Antibacterial Activity ◽  
Saudi Arabia ◽  
Oral Hygiene ◽  
Leaf Extract ◽  
Radical Scavenging Activity ◽  
Radical Scavenging ◽  
Scavenging Activity ◽  
Reference Drug ◽  
Wide Range ◽  
Peel Extract

Commiphora gileadensis is commonly used in Saudi Arabia for oral hygiene. A lack of data about its biological activity encouraged us to evaluate the antioxidant and antibacterial activities of its leaf and stem extracts. Ethanol, methanol, acetone and deionized water were tested as extraction solvents. 80% methanol gave the highest extracted concentrations of phenolic and flavonoid substances. The leaf and stem extracts were respectively evaluated for their radical scavenging activity with DPPH (EC50 = 3.39, and 1.06), ABTS (EC50 = 0.690, and 0.55), and peroxide scavenging activity (EC50 = 2.43, and 1.28). GC-MS identified a wide range of compounds that may be responsible for these activities of the results observed. The highest levels of chlorophyll, carotenoids, and lycopene were found in the leaf extract while level of proanthocyanidins was found in the stem peels extract. The peroxidase and catalase activities of stem peel extract were higher than those of the leaf extract. The findings showed that the leaf and stem peel extracts of C. gileadensis exhibited significant antibacterial activity against the test organisms. The minimum inhibitory concentrations for the plant extracts were compared with the standard reference drug Augmentin but the time–kill curves for the C. gileadensis extracts showed that they were less effective than Augmentin. Moreover, the stem peel extract exhibited stronger antibacterial activity than the leaf extract. In conclusion, C. gileadensis can be an important source of natural antioxidants, used as a healthy chewing stick for teeth brushing and oral hygiene purposes.

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