Citrus aurantium for immune system -
Amyloid beta Aβ is generated from the cleavage of amyloid precursor protein APP by the combination of enzymes, β-secretase, and γ-secretase. Aβ 1—42 protein is a fragment of the full-length Aβ that can cause inflammation and synaptic toxicity by initiating different biochemical cascades 8 , 9.
In addition to Aβ accumulation, hyperphosphorylation of the tau protein is a pathological feature observed in AD that triggers the neurodegenerative process Furthermore, memory dysfunction is also triggered by cholinergic system damage that includes cholinergic neurons, neurotransmitters, and their receptors 5 , Therefore, it is important to maintain the acetylcholine Ach level by inhibiting the acetylcholinesterase AchE activity.
Various AchE inhibitors such as tacrine, donepezil, rivastigmine, and galantamine have been used to treat cognitive impairment by inhibiting AchE activity at the cholinergic synapses and thus, increasing the Ach content.
However, the clinical efficacy remains unexplored; moreover, various side effects have been reported Citrus fruits have been traditionally used as medicine to increase immunity, alleviate indigestion, and reduce inflammation in Asia The peels of Citrus aurantium contain a variety of active components, including naringin, hesperidin, narirutin, and polymethoxylated flavone PMF such as nobiletin and tangeretin.
Previous studies, reported that nobiletin has various biological properties such as anti-cancer activity, anti-oxidant capacity, anti-inflammatory effects, and anti-obesity activity 13 — 15 as well as anti-dementia activity However, this has not yet been tested on memory loss in an Aβ 1—induced normal mouse model.
The nobiletin concentration was determined by calculating the amount of nobiletin contained in the CAE in this experiment. We hypothesized whether CAE and nobiletin treatments have similar anti-dementia effects and underlying anti-apoptotic activity against β-amyloid-induced memory impairments in mice.
The CAE was supplied by KPLC Group Paris, France and prepared as described previously. The main component of CAE, nobiletin, was analyzed by high-performance liquid chromatography according to followed method: The solvent was a mixture of water A and Methanol B and delivered at 0.
Osaka, Japan. Seongnam, South Korea. After a 7-day acclimation period, they were used in the experiment. All experiments were approved by an Ethics Committee no. Yongin, Korea and performed in accordance with the national guidelines for the care and use of laboratory animals and the mice were maintained according to their guidelines.
We monitored changes in body weight once a week, and observed changes in feed and water intake. In additions, appearance changes such as hair coat, activity, and posture were monitored once a day after β-amyloid injection over the course of the experiments. To improve animal well-being, we provided a sanitary environment to prevent disease and proper breeding and management and used appropriate painkillers and anesthetics to reduce pain.
The humane endpoints were set by observing body weight change, hair coat, movement and posture of mice and applied in consultation with experimental committee. When both sings as lack of respiration and faded eye color were observed, the mice were removed from the CO 2 chamber. Aβ 1—42 was dissolved in sterile 0.
The respective drugs were given orally p. for 4 weeks Day Based on the results of previous studies, the concentrations of CAE and nobiletin were set 3 , 13 , The passive avoidance test was conducted in all groups for 3 days Days 15—17 and Morris water maze MWM task for 7 days Days 22— The mice were performed by cardiac puncture for exsanguination after carbon dioxide anesthesia at Day 28 and were confirmed the death by observing stop breathing and cardiac dysfunction through CO 2 anesthesia and exsanguination.
The entire experimental schedule is shown in Fig. To determine learning and memory ability, the passive avoidance test was conducted in an acrylic shuttle box with two compartments and a guillotine door in the middle.
The box consists of illuminated and non-illuminated compartments with an electric grid floor that allows for electronic shock stimuli. The test was performed on 3 consecutive days at h intervals.
On the first day Day 15 , the animals were allowed to explore the non-illuminated compartment for 2 min and then transferred back to the illuminated compartment. They were then allowed to access the illuminated and non-illuminated compartment freely for 60 sec.
If the mice moved to the non-illuminated compartment, they were immediately removed and trained to adapt to the illuminated compartment.
After the end of adaptation the time, on the second day, the mice moved between the two compartments for sec, but when they entered the non-illuminated compartment, the guillotine door automatically closed and a scrambled shock was given for 2 sec.
On the last day of the test, Day 17, the mice were placed in the illuminated compartment and the time taken for them to move to the non-illuminated compartment after the door opened was measured. On Day 22, the mice were tested using the MWM task.
A circular water pool was divided into quadrants; the platform was randomly located within one quadrant. The mice were trained to find the platform for 60 sec. When the mice reached the platform, they were allowed to remain on the platform for 30 sec; if they could not find the platform within 60 sec, they were guided and placed on it for 30 sec to learn the extra maze cues.
All animals performed two trials per day and the position of the platform in the circular pool was randomly changed. The task consisted of 2 days of training; 4 days of acquisition, during which the time to find the platform was recorded; and 1 day of probe trial.
For the probe trial, the platform was removed and the animals were allowed to search it for 1 min. The number of crossings by the mice in the quadrant with the removed platform was measured on Day At the end of the experiment, the mice were sacrificed, and the cortex and hippocampus were dissected from the brain.
Both tissues were rapidly homogenized and sonicated in 0. AchE activity was determined using commercial assay kits Abnova; cat. KA, Taiwan according to the manufacturer's instructions.
The activity was calculated as the optical density OD at nm and represented as OD values per milligram of protein. The dissected cortex and hippocampus tissues were lysed in radioimmunoprecipitation assay buffer containing 50 mM Tris-HCl pH 7.
The supernatant was collected, and the protein concentration was calculated by bicinchoninic acid protein assay kit Thermo, USA. The membranes were blocked with commercial blocking buffer Thermo, USA for 1 h at room temperature and washed thrice with Tris-buffered saline containing 0. After washing, the membrane was incubated at 4°C overnight with the following appropriate antibodies: B-cell lymphoma 2 Bcl-2 -associated X protein Bax; ,; cat.
The membranes were again washed thrice and enhanced using chemi-luminescence reagents. The protein bands on the membrane were detected by a chemi-luminometer ATTO, Japan.
Densitometry was performed using the Image-Pro Plus soft-ware version 6. Data are expressed as the mean ± standard error and were analyzed with SPSS Statistics Different treatment groups were compared using one-way analysis of variance followed by multiple comparisons using Dunnett's post hoc test using Origin 7.
The composition in CAE were investigated the chromatographic profiles of a standard on HPLC analysis. The optimized CAE was used in all subsequent experiments. The mice did not show any change in body weight during the experiment, but hair coat showed rough condition.
Response to weak stimuli decreased and activity ability also decreased. Also, the mice was sitting on the floor with a curved posture was observed and through these symptoms, the humane endpoint was set. The animals were sacrificed by meeting the defined endpoint.
The effect of CAE and nobiletin on the Aβ 1—induced memory impairment was measured using a passive avoidance task. The step-through latency of the Aβ 1—only treated group was significantly shortened compared to the control group Fig.
However, the reduced step latency with Aβ 1—42 was restored by the administration of CAE and nobiletin. Effect of nobiletin and CAE on step-through latency in passive avoidance test in Aβ 1—42 induced memory impairment. The data are presented as mean ± standard error of the mean.
Aβ, amyloid β; CAE, Citrus aurantium extract. The efficacy of CAE and nobiletin in protection from the spatial memory impairment via Aβ 1—42 injection was further confirmed.
The escape latency assessment was performed twice a day. During the test period, escape latency decreased slightly in the second trial compare to the first trial in all experimental groups Fig. No difference was observed in the escape latency for 4 days in the amnesic mice, which were treated with Aβ 1— By contrast, the control group showed significantly decreased escape latency in two trials over 4 days Fig.
It is well-established that Aβ 1—42 induces memory loss and increases the escape latency. Similarly, the escape latency in mice administered nobiletin significantly decreased for 4 days compared to the Aβ 1—only injected group.
Effect of nobiletin and CAE on Aβ 1—42 induced memory impairment in the Morris water maze. The escape latency of A Trial 1 and B Trial 2, and the mean of C Trial 1 and Trial 2 during the training sessions for 4 days. The effect of CAE and nobiletin treatment on the swim distance to locate the platform in the MWM task is shown in Table I.
The control group mice were able to swiftly locate the platform and reached the platform during the training session. However, the Aβ 1—treated group had difficulty learning to locate the platform. The swim distance was significantly increased compared to that of the control group.
The mice in the nobiletin-treated group were also able to find the platform easily with a short swim distance, especially on Day Effect of nobiletin and CAE on the distance swum by Aβ 1—42 treated mice to find the platform in the water maze task.
To evaluate the spatial memory of the mice, the number of crossings to the platform was measured in the probe trial on Day As shown in Fig. These results show that these drugs enhance spatial cognition, learning, and memory functions against Aβ 1—induced memory impairment. Effect of nobiletin and CAE on the number of crossing in a probe trail on Day To investigate the neuroprotective effect of CAE and nobiletin on brain tissue, AchE activity was measured in the cortex and hippocampus Table II.
The AchE activity in the Aβ 1—treatment group was significantly increased compared to that in control group. Similarly, the AchE activity in the nobiletin treatment group also decreased significantly by The effect of CAE and nobiletin on the Bcl-2 family and caspase pathway was investigated in the cortex and hippocampus.
In contrast, Bcl-2 protein expression was higher in the control group than in the Aβ 1—only treated group in the cortex and hippocampus. A similar protein expression pattern was observed in the cortex. Effect of nobiletin and CAE on protein expression in A hippocampal and B cortex tissues.
The expression was detected by western blot analysis. Bax, Bcl-2 and cleaved caspase-3 protein levels were normalized by separate control β-actin, respectively.
Aβ, amyloid β; CAE, Citrus aurantium extract; Nob, Nobiletin. The present study is the first report to evaluate the neuroprotective effects in Aβ 1—induced memory impairment animal model and not the transgenic or senescence accelerated mouse model. Our results showed that the Aβ 1—injection resulted in severe performance deficits in the passive avoidance and Morris water task as well as neurodegeneration in the mice brain that was evident from increased AchE activity in the hippocampus and cortex.
In this study, we treated the amnesic mice with CAE and nobiletin and confirmed the anti-amnesic effect by regulating of apoptotic signaling. Aβ plays a major role in the development of AD, particularly the neurotoxic Aβ 1—42 The direct injection of Aβ 1—42 in the rodent brain has been used to cause apparent memory deficits, and Aβ-exposed rats have shown hippocampus-dependent spatial learning dysfunction in long and short-term tasks 4.
Also, the brains of AD patients demonstrated a high Aβ level compared with normal aged brain samples The deposition of Aβ in the cortex and hippocampus, which are responsible for learning and memory performance, resulted in neuronal apoptosis 21 , To examine the protective effect of CAE and nobiletin, we performed the passive avoidance and MWM tasks to investigate learning and memory function.
The passive avoidance task is a method that is used to measure the escape time from the space that induces pain and fear by electronic shock in rodents It is commonly used to confirm the memory function, and we found in this study that CAE and nobiletin administration significantly increased the step-through latency to similar levels, a phenomenon that was reduced by the Aβ 1—42 injection.
The MWM is an assessment method to evaluate hippocampal-dependent learning abilities and cognitive deficits in rodents. The animals were trained to learn spatial working information at the learning stage and assisted to build future memory These results are consistent with those of previous studies that show Aβ-induced memory deficits in an MWM task than those in the saline group As a result of two trials for 4 days on the MWM task, CAE treatment reduced escape latency in the second trial compared to the first trial, and escape time decreased over training days.
The nobiletin administration group showed similar escape latency for 4 days in the first trial, and the escape latency decreased rapidly on Day 26 in the second trial. Although the pattern of escape latency of the CAE and nobiletin group was slightly different, the mean escape latency was decreased to a similar pattern.
This means that CAE and nobiletin administration showed significant decreases in escape latency, improvement in cognitive performance, and amelioration of the memory deficits.
Furthermore, to investigate the neuroprotective effect of CAE and nobiletin, we examined the changes in the Ach system in the hippocampus and cortex. Ach is an essential enzyme that maintains the normal function of the nervous system and is hydrolyzed by AchE.
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Citrus Allergen control solutionscommonly referred aurantiu, as sour orange or bitter orange, holds significant Aystem both in biological and economic fo. Throughout history, humans have turned to immue in vor pursuit of health Citrus aurantium for immune system wellness. Among the plants that have historically played a role in enhancing fitness, Citrus aurantium stands out. A diverse array of phytochemical constituents present in Citrus aurantium have been closely tied to its various biological activities, encompassing areas such as gastrointestinal disorders, insomnia, headaches, cancer treatment, antiseptic properties, antioxidant effects, and antispasmodic effects. Beyond its pharmacological relevance, Citrus aurantium also boasts numerous non-pharmacological applications that make it particularly intriguing.Citrus aurantium for immune system -
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Try again? Furthermore, one study determined that bitter orange juice contains furanocoumarin, a compound that may cause the same medication interactions as grapefruit juice Therefore, people taking decongestants or those who have high blood pressure, an irregular heartbeat, or glaucoma should avoid the juice and fruit of bitter oranges.
Despite numerous studies showing that bitter orange extracts are not stimulants, widespread controversy exists, and the NCAA has listed it as a banned substance. Bitter orange may also interact with certain medications. Generally, bitter orange extracts in dietary supplements are safe to consume in doses of 50—98 mg per day 1 , One study showed that 40 mg of synephrine combined with mg of caffeine is a safe dose of these combined ingredients 3.
In another study, eating a whole bitter orange containing Still, people who are pregnant or breastfeeding should avoid bitter orange due to a lack of safety information 1.
Bitter orange is likely safe in doses ranging from The juice of the bitter orange can be used as a marinade to flavor fish and meat. Bitter orange has several other household uses outside of the kitchen.
These include 2 :. Bitter orange is a citrus fruit with several household and industrial uses, ranging from food additives to perfumery. You may want to avoid this fruit and its extracts if you have high blood pressure, an irregular heartbeat, or glaucoma. Likewise, bitter orange supplements are banned for NCAA athletes.
Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available. Some argue that orange peels contain important nutrients and should be eaten rather than thrown away.
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Some studies suggest vaping may help manage your weight, but others show mixed…. The amount of time it takes to recover from weight loss surgery depends on the type of surgery and surgical technique you receive.
New research suggests that running may not aid much with weight loss, but it can help you keep from gaining weight as you age. Here's why. A Quiz for Teens Are You a Workaholic? Many immune cells express vitamin D—activating enzymes allowing them to convert vitamin D precursors to the active form of vitamin D.
Multiple studies have found associations between low vitamin D and increased risk of infections, including influenza and other respiratory infections and sepsis.
However, many other studies showed positive benefits of vitamin D on respiratory infection, particularly in people with low vitamin D status. Fortified orange juice varieties often provide vitamin D along with calcium needed for strong bones.
Research supports the role of flavonoids in the immune system. In human clinical studies, hesperidin in orange juice exerted positive changes in antioxidant enzymes, altered white blood cell gene expression to anti-inflammatory profiles, and lowered oxidative stress biomarkers that protect against DNA damage and lipid peroxidation.
The flavonoid hesperidin is highly concentrated in citrus and rarely found in other foods, 15 making orange juice a unique source.
Consider including nutrient-rich Florida Orange Juice in your daily diet. Working to maintain a healthier immune system is also a great way to help you get through cold and flu season.
FDA rounding rules applied when calculating percent DV based upon rules. Information is not intended for labeling food in packaged form. Nutrient values may vary based on brand or product types. Privacy Policy Terms of Use. Florida Citrus Florida Orange Juice Menu. FOR INDUSTRY.
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Orange extract is extracted fog the orange peel. The Citrus aurantium for immune system is used syste, improve digestion, relieve intestinal gas immunr bloating, and Cranberry BBQ sauce recipes. It is one of the greatest sources of vitamin C, and it enhances the immune system and helps to decrease infections. Orange peels are the histamine and anti-inflammatory properties, which are useful for lung cleansing. Orange extract is a great herbal medicine for asthma and pneumonia. Bitter Citrrus Citrus aurantiumalso known as sour orange aurahtium Seville orange, is a citrus fruit Hyperglycemia and type diabetes a multitude of Citrus aurantium for immune system. This Citus covers Ofr you need to know auranhium bitter fof, including its role in weight loss and skin health, as well as its overall safety as a supplement. The bitter orange plant thrives in subtropical regions but can withstand adverse environmental conditions like frost for short periods 2. Oval or oblong in shape, the fruit is red-orange when ripe and has a distinctively thick, dimpled skin. There are 23 cultivars of the fruit, the most prominent of which is Bergamot. You can expect some varieties to be more bitter than others.
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