{"id":55202,"date":"2023-12-31T10:02:48","date_gmt":"2023-12-31T10:02:48","guid":{"rendered":"https:\/\/biomedpharmajournal.org\/?p=55202"},"modified":"2024-04-16T10:18:47","modified_gmt":"2024-04-16T10:18:47","slug":"protective-effect-of-prosopis-farcta-fruit-aqueous-extract-against-oxidative-stress-caused-by-ethanol-in-albino-rats","status":"publish","type":"post","link":"https:\/\/biomedpharmajournal.org\/staging\/vol16no4\/protective-effect-of-prosopis-farcta-fruit-aqueous-extract-against-oxidative-stress-caused-by-ethanol-in-albino-rats\/","title":{"rendered":"Protective Effect of Prosopis Farcta Fruit Aqueous Extract Against Oxidative Stress Caused By Ethanol in Albino Rats"},"content":{"rendered":"\n

Introduction<\/strong><\/p>\n\n\n\n

Prosopis farcta<\/em>, or Syrian mesquite, is a flowering herb native to\nAsia and belongs to the Fabaceae family.1<\/sup> P. farcta <\/em>fruitscontain\nvarious bioactive compounds; for this reason, they have been used in traditional medicine in many\nAsian countries.1,2<\/sup> The fruit extract contains 99.2% of the\nessential substances and bioactive chemicals, such as gallic and vanillic\nacids, alkaloid compounds, quinones, phenol compounds, glycosides, tannins,\ntriterpenoids, and phytochemical compounds of natural antioxidants, for use in\nbiomedicine and the food industry.2,3<\/sup> The phytochemical composition,\nC-glycosyl flavone content, is increasingly associated with the observed\nbiological effects. Epidemiological research has proposed an opposite relationship between the expenditure of these phytochemicals\nand a decreased risk of complications, such as certain disorders\nor chronic.2<\/sup> The dried\nfruits have been used to treat various ailments, including kidney stones.4<\/sup> asthma,\ncalluses, diabetes, diarrhea, scabies, otitis, rheumatism, abdominal pain (ulcer),\nfever, flu, breastfeeding, liver infection, malaria, conjunctivitis, pancreatic\nstones, and cardiovascular conditions.2<\/sup> pregnancy, newborn illnesses, skin wounds,\nand burns.5<\/sup> Furthermore, the therapeutic\nbenefits of diabetic foot ulcers, laryngitis, and dyspnea have been\ndemonstrated. It also has\nantispasmodic, anti-inflammatory, and pain-relieving properties.6<\/sup> Possess fascinating\nantispasmodic, antipyretic, cancer-fighting, antidiabetic, and wound-healing\nproperties.7<\/sup> According\nto several studies, both in vivo and in vitro, antioxidant, antimicrobial, and\nanticancer activities were discovered in an experiment.8<\/sup> The\nfindings also stated that its high\nconcentration of phenols and flavonoids is directly responsible for its antioxidant\nproperties.9<\/sup> The\nn-butanol, ethyl acetate, and 5-fluorouracil extracts of the aerial parts of P.\nfarcta<\/em> were estimated to have anticancer vitality against many lines of\ntumor cells in humans.10<\/sup><\/p>\n\n\n\n

Alcohol intake, non-steroidal\nanti-inflammatory drugs, cigarettes, a poor diet, and physical and psychological\nstress usually lead to stomach ulcers.11<\/sup>\nThese factors may cause oxidative stress.12<\/sup> Ethanol\nleads to ulceration of the gastric mucosa through the production of extremely\nharmful free radicals and their effect as a necrotic agent.13<\/sup> Because\nethanol interferes with stomach mucus secretion, alters the permeability of\nendothelial cells (mucosa), and reduces mucus secretion, gastric mucosal cells\nbecome more vulnerable to free radicals.14<\/sup> Oxidative\nstress (OS) is the mismatch between pro-oxidant processes brought on by\nreactive oxygen species (ROS) and an organism’s ability to fend off their\nexcessive synthesis or deal with the fallout from them. Numerous studies have\ndemonstrated that elevated ROS generation in gastrointestinal diseases causes\ninflammation and increases ROS creation.15,16<\/sup>\nThe current study might offer a quick and safe way to alleviate the\ninflammation brought on by large doses of ethanol in rats using three different\nconcentrations of the aqueous extract from the fruits of P. farcta<\/em>.<\/p>\n\n\n\n

Materials and Methods<\/strong><\/p>\n\n\n\n

Extract preparation <\/strong><\/p>\n\n\n\n

Dried fruits of Prosopis farcta <\/em>were purchased\nfrom the Ibn Sina’s herbarium, Al Nasr District Street, Kerbela, Iraq. The P.\nfarcta<\/em> fruit aqueous extract\n(PFFAE) is a standardized water extract from P.\nfarcta <\/em>fruits. The fruits were cleaned, the cores\nwere separated, and a mechanical grinder was used to smash the fruits into a\nfine powder. The 500-gram powdered fruit sample was disintegrated in 500 mL of purified\nwater and left to stand for 24 hours at room temperature (25 \u00b1 2 \u00b0C) before being filtered. After that,\nthe filtrate was put into a stainless-steel plate, where the extract was dried\nfor 12 hours at 30 \u00b0C in the oven.17<\/sup> The\nconcentrated extract was kept in refrigerators in clearly marked containers\nuntil it was required for the study. The final product was the crude extract,\ndiluted with distilled water and given to the rats. Ethanol was purchased from Reflecta Laboratory\nSupplies, South Africa. All other reagents utilized on the practical side were\nof analytical grade. <\/p>\n\n\n\n

Animals and experimental protocol<\/strong><\/p>\n\n\n\n

Thirty-two male Rattus\nnorvegicus<\/em> with an average\nweight of 180\u2013200 g were used. The current study obtained animals from the animal\nhouse of the College of Pharmacy \/ University of Karbala. The procedure\ncomplies with National Institutes of Health (NIH) requirements, and the local\ncommittee approved the research design. The animals were kept in groups of four\nin cages, with unlimited access to food and water. Following two weeks of\nacclimation, the animals were split into four equal groups: group I (control) was treated with distillation water; group\nII (ethanol) was dosed with 35% ethanol for 0.005 ml\/g to induce inflammation\n(Abdel-Kawi et al. 2022),18<\/sup> Group III were orally treated with PFFAE (400 mg\/kg bw),19<\/sup> after one hour of dosing with 35% ethanol at 0.005 ml\/g. Group IV was\norally treated with PFFAE (300\nmg\/kg bw),20<\/sup> after one hour of dosing with 35% ethanol at 0.005 ml\/g. All groups were\norally administered for 30 consecutive days.<\/p>\n\n\n\n

Experimental parameters<\/strong><\/p>\n\n\n\n

The C-reactive protein (CRP) and albumin\nwere measured using Rat CRP and Albumin Detection Kits from Chondrex (USA), and\nthe CRP\/albumin ratio This ratio is called “APRs.” It is calculated\nby dividing the level of CRP by the albumin level,21<\/sup> erythrocyte sedimentation rate (ESR),\nwhite blood cell (WBC) leucocyte count measured by using BC-3000Plus hematology\nmachines Mindray (India), malondialdehyde (MDA) measured by using Dojindo’s MDA\nAssay Kit (Japan), and glutathione peroxidase (GPx) measured by using the rat\nglutathione peroxidase (GPX) ELISA Kit Siga-Aldrich (Germany).<\/p>\n\n\n\n

Statistical analysis<\/strong><\/p>\n\n\n\n

The statistical significance among the groups was evaluated\nusing IBM SPSS Statistics (22.0) and a one-way ANOVA table. A P-value of less\nthan 0.05 (P < 0.05) was considered significant. The least significant\ndifference was taken to verify the validity of the observed effects.<\/p>\n\n\n\n

Results <\/strong><\/p>\n\n\n\n

Table 1: Parameters assessment in various experimental groupings.<\/strong><\/p>\n\n\n\n\n\n\n\n\n\n
\n

groups<\/strong><\/p>\n<\/td>\n

\n

CRP (mg\/dl)<\/strong><\/p>\n<\/td>\n

\n

Albumin (mg\/dl)<\/strong><\/p>\n<\/td>\n

\n

CRP\/ALB ratio<\/strong><\/p>\n<\/td>\n

\n

ESR mm\/hr<\/strong><\/p>\n<\/td>\n

\n

MDA (\u00b5mol\/l)<\/strong><\/p>\n<\/td>\n

\n

GPx (IU\/l)<\/strong><\/p>\n<\/td>\n

\n

WBC (x103\/\u03bcL) <\/strong><\/p>\n<\/td>\n<\/tr>\n

\n

Group I<\/strong><\/p>\n<\/td>\n

\n

0.10 \u00b1 0.00<\/p>\n<\/td>\n

\n

4.46 \u00b1 0.38<\/p>\n<\/td>\n

\n

0.21 \u00b1 0.01<\/p>\n<\/td>\n

\n

2.00 \u00b1 0.00<\/p>\n<\/td>\n

\n

1.12 \u00b10.12<\/p>\n<\/td>\n

\n

47.16 \u00b1 1.40<\/p>\n<\/td>\n

\n

04.00 \u00b1 0.42<\/p>\n<\/td>\n<\/tr>\n

\n

Group II<\/strong><\/p>\n<\/td>\n

\n

1.05 \u00b1 0.29\u1d43<\/p>\n<\/td>\n

\n

2.40 \u00b1 0.38\u1d43<\/p>\n<\/td>\n

\n

0.45 \u00b1 0.15\u1d43<\/p>\n<\/td>\n

\n

2.00 \u00b1 0.00<\/p>\n<\/td>\n

\n

2.93 \u00b1 0.5\u1d43<\/p>\n<\/td>\n

\n

38.76 \u00b1 0.57\u1d43<\/p>\n<\/td>\n

\n

14.11 \u00b1 0.99\u1d43<\/p>\n<\/td>\n<\/tr>\n

\n

Group III<\/strong><\/p>\n<\/td>\n

\n

0.60 \u00b1 0.33\u1d43\u1d47<\/p>\n<\/td>\n

\n

2.70 \u00b1 0.23\u1d43<\/p>\n<\/td>\n

\n

0.23 \u00b1 0.14\u1d43\u1d47<\/p>\n<\/td>\n

\n

2.50 \u00b1 0.55\u1d43\u1d47<\/p>\n<\/td>\n

\n

3.05 \u00b1 0.40\u1d43\u1d47<\/p>\n<\/td>\n

\n

32.41 \u00b1 1.17\u1d43<\/p>\n<\/td>\n

\n

09.58 \u00b1 0.88\u1d43\u1d47<\/p>\n<\/td>\n<\/tr>\n

\n

Group IV<\/strong><\/p>\n<\/td>\n

\n

0.17 \u00b1 0.07\u1d47<\/p>\n<\/td>\n

\n

3.77 \u00b1 0.08\u1d43\u1d47<\/p>\n<\/td>\n

\n

0.04 \u00b1 0.02\u1d47<\/p>\n<\/td>\n

\n

2.50 \u00b1 0.55\u1d43\u1d47<\/p>\n<\/td>\n

\n

1.77 \u00b1 0.15\u1d43\u1d47<\/p>\n<\/td>\n

\n

41.75 \u00b1 1.17\u1d47<\/p>\n<\/td>\n

\n

07.56 \u00b1 1.11\u1d43\u1d47<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n\n\n

The values are clearly mean \u00b1 SD value, n = 6\nin each group, \u1d43 show the difference in statistics. With a control group, \u1d47 statistical\ndisparity according to illness group, (P < 0.05).<\/p>\n\n\n\n

Table 1 showed\nsignificant differences in blood parameter levels, i.e., ethanol group 2. The experiment’s\nblood parameters (CRP, CAR, MDA, GPx, ESR, WBC, and albumin) may be altered by\nethanol. While there was a significant increase (P < 0.05) between the\nethanol group II and the low-concentration treatment group (III) compared to\nthe control group, there were no discernible differences in the levels of CRP\nbetween the treatment groups (IV and V) and the group I (control) (P = 0.05),\nwhich could be explained by Group II’s high level of ethanol-induced\ninflammation.<\/p>\n\n\n\n

All study\ngroups had significantly lower albumin levels than the control group (P >\n0.05), and the II and III groups had lower albumin levels than the IV and V\ngroups. Table 1 indicated no significant differences in the albumin\/CRP ratio\nbetween Groups IV and V and Group I (P = 0.05). There is a significant rise (P\n< 0.05) compared to the control group, in contrast to the II and III groups.\nCompared to other parameters, the ESR levels showed a significant increase (P\n< 0.05) in groups III, IV, and V compared to group I; however, there were no\nsignificant differences (P = 0.05) between groups III, IV, and V and group II\nand the control group on the other hand. <\/p>\n\n\n\n

Regarding the\nWBC count, it was found that all research groups saw a substantial increase (P\n> 0.05), especially in group (I) findings. In contrast, the IV and V groups\nexperienced a significant reduction (P > 0.05) compared to the II and III\ngroups. Ultimately, the findings showed that, in comparison to the control\ngroup, all research groups had significantly higher MDA rates (P < 0.05);\nhowever, group II saw a significantly lower MDA rate (P > 0.05) in the IV\nand V groups. All experimental groups, including group II (ethanol), had lower\nMDA values than the treatment group with the lowest concentration. All study\ngroups had considerably lower levels (P > 0.05) of GPx than the control\ngroup, whereas groups IV and V had significantly greater levels (P > 0.05)\nthan groups II (ethanol) and III.<\/p>\n\n\n\n

Discussion<\/strong><\/p>\n\n\n\n

The\neffect of ethanol on the Blood parameters levels:<\/strong><\/p>\n\n\n\n

We observed a notable rise in the level of C-reactive protein\nin group II as opposed to other experimental groups, which confirms the role of\nethanol in stimulating inflammatory factors, which in turn increase C-reactive\nprotein levels.22<\/sup> This is also the case for substances. The levels of\nmalondialdehyde oxidation and the number of red blood cells increased in this\nsecond group as opposed to the experimental and control groups. Ethanol\nstimulates oxidative stress through the production of ROS 23<\/sup> and plays a crucial role in many diseases, such as gastric\nulcers.24<\/sup> <\/strong><\/p>\n\n\n\n

The\neffect of P. farcta<\/em> extract on the CRP level:<\/strong><\/p>\n\n\n\n

The\nCRP levels gradually decreased in the treatment groups (III, IV) that received amounts\nof 0.15, 0.30, and 0.45 mg\/kg of P. farcta extract after receiving 0.005 ml\/g\nof 35% ethanol; this indicates that the aqueous extract lessened the effects of\nethanol in these groups relative to group II, and the lower concentration of\nthe aqueous extract in the treatment group III, 0.15 mg\/kg, had less effect on\nthe CRP level.<\/p>\n\n\n\n

CRP is broadly utilized as an\nindicator for the diagnosis and control of inflammation\nand tissue\ndamage involving sepsis, trauma, and malignancies.25<\/sup> CRP secondary effects that come after binding share some of\nthe primary characteristics of antibodies, acting as an inflammatory medium and\nbolstering the host’s defense against infection.26<\/sup> Rats myocardial infarction has been seen as direct evidence\nof its role in exacerbating tissue damage as a result of its inflammatory\neffect,27<\/sup> and the fact that levels of CRP are an indicator of the\npresence of inflammation,28,29<\/sup> therefore, its decrease in the groups of 0.30 and 0.45 mg\/kg\nconcentration of aqueous extract of P. farcta<\/em> is evidence of its role as\nan anti-inflammatory,5<\/sup> caused by ethanol, which increases the liver’s synthesis of\nCRP.30<\/sup> Half of CRP is about 19 hours old in the bloodstream and\nincreases within 6 hours of inflammation or tissue damage. It peaks within 2\u20133 days of the onset of inflammation but declines rapidly as the state of\ninflammation disappears.31<\/sup> This explains its low level in III, IV, and V groups as opposed to its counterpart in ethanol group II.<\/p>\n\n\n\n

The\neffect of P. farcta<\/em> extract on the Albumin level:<\/strong><\/p>\n\n\n\n

Albumin levels considerably dropped in group II due to the ethanol while\nremaining unaffected in group III, which received the smallest dose of 0.15\nmg\/kg of the aqueous extract of P. farcta. However, the levels of albumin in\nthe IV and V treatment groups that received doses of 0.30 and 0.45 mg\/kg of P.\nfarcta<\/em> extract after receiving 0.005 ml\/g of 35% ethanol showed a\nsignificant increase, which indicates that the extract’s effects are visible in\nthe rise in albumin levels in these two groups. <\/p>\n\n\n\n

Albumin plays an essential role in\nphysiology by distributing body fluids, regulating basal acid balance,\ninhibiting the functioning of platelets and vascular permeability, maintaining\nosmosis pressure32<\/sup>, and binding essential ingredients in the bloodstream.33<\/sup> Furthermore, a result of being prescribed properties as an\nantioxidant by trapping free radicals,34<\/sup> compared to the CRP that rises in inflammation, and because\nthe half-life of albumin is 19 days,35<\/sup> it gradually decreases from\nthe moment inflammation begins, especially in hepatocytes, whose levels may\nindicate a wide range of conditions and diseases, including kidney disease,\nliver disease, malnutrition, inflammation, and cancer36<\/sup>; therefore, doctors may use it to\nevaluate the nutrition of patients and follow up on infections that cause a\nsignificant decrease in its concentration,37<\/sup> a decrease in serum albumin (< 3.5 g\/dL) is often due to\nthe death of hepatocellular cells resulting from chronic liver disease and\nimpaired albumin synthesis; a decrease in its level in inflammatory cases is\nexpected; and it has been proposed that this product plays a crucial role in\nreducing production during inflammation.38,39<\/sup> The decreased albumin level in the ethanol group II\nindicates hepatocyte damage. In contrast, the beginning of its gradual rise in\nthe therapeutic groups of 0.30 and 0.45 mg\/kg concentration of aqueous extract\nof P. farcta<\/em> indicates an improvement in the physiological condition of\nthese groups due to the effect of this extract.<\/p>\n\n\n\n

The\neffect of P. farcta<\/em> extract on the CAR level:<\/strong><\/p>\n\n\n\n

In the current investigation, the albumin\/CRP ratio was determined to\ncorroborate the findings that the levels of albumin and CRP are inversely\ncorrelated. Recent works have focused on the interactions between\nalbumin and CRP. For example, the ratio of albumin to CRP, i.e., CAR, is considered a new biomarker of clinical\nconditions.40<\/sup> More\nrecently, CAR was examined in patients with several types of malignant tumors,41<\/sup> and in the\ncontext of cardiovascular disease,42<\/sup> by linking\nthe adjusted early warning index (MEWS) with the CAR ratio for rapid diagnosis\nof these critically ill patients.43<\/sup> The CAR is\ncommonly used as a factor to measure the activity of inflammatory cases and\ndetermine the degree and activity of inflammatory disease with a consistent\nrecording system, which is a more useful indicator of inflammatory cases than\nthe measurement of CRP or albumin in isolation.44<\/sup> Its elevation was found in\nacute pancreatitis patients; the CAR was calculated in the current study to\nsupport the results of the level of CRP and albumin, which are inversely\nproportional.45<\/sup> As a result, the P. farcta<\/em> extract’s impact on the\nCAR is still obvious because it follows from its impact on CRP and albumin.<\/p>\n\n\n\n

The\neffect of P. farcta<\/em> extract on the ESR level:<\/strong><\/p>\n\n\n\n

Because of ESR’s slow reaction to inflammation due to its poor\nsensitivity to simple inflammation, the initial rise starts within 24\u201328 hours\nand drops once inflammation resolves. It cannot diagnose disease due to its\nslow response to inflammation.46<\/sup> ESR is known\nto be impacted by an extensive array of physiological and pathological factors\nthat include not only changes in the concentration of fibrinogen in plasma but\nalso changes in the size, shape, and number of aqueous chloride, as well as the\npresence of acute-phase reaction proteins (such as immunoglobulin).47<\/sup> and for the speed at which it is affected by the\nfactors caused by the disease (inflammation), so it is expected that there will\nbe a variation between its rates in all experimental groups; in other words, it is a non-specific indicator of diseases, and since\nour current study did not include inducing a specific disease in itself but\nrather an inflammatory response produced by the high and repeated concentration\nof ethanol, Therefore, when designing the experiment, several considerations\nwere considered. The most important was the selection\nof male laboratory animals for the sensitivity of ESR to physiological factors\nbetween females and males on the one hand, between pregnant females, the period\nof menstruation, and natural females on the other hand.48<\/sup> Success in\ntreating many diseases depends on early recognition of the patient’s condition.\nThe ESR is a valuable test for this purpose.49<\/sup> In addition,\nthe induction of a pathological condition in healthy and medium-life laboratory\nrats with alcohol may not be sufficient to stimulate severe inflammatory\nconditions that raise ESR levels, especially since this is a biomarker that is\noften used to assess and follow up on specific conditions such as rheumatic\narthritis.50<\/sup> Finally, due\nto the presence of more sensitive and specific inflammatory biomarkers, ESR is\noften not recommended as an examination test.51<\/sup> There was no\nclear effect of P. farcta<\/em> on the ESR level in the present study; ESR was\nnot affected by the high doses of ethanol. <\/p>\n\n\n\n

The\neffect of P. farcta<\/em> extract on the WBC count:<\/strong><\/p>\n\n\n\n

The increasing count of WBC in the ethanol group II was gradually\nreduced when they received amounts of 0.15, 0.30, and 0.45 mg\/kg of aqueous\nextract of P. farcta<\/em> after receiving 0.005 ml\/g of 35% ethanol, to the\npoint where there was a considerable decrease in it compared to the ethanol\ngroup II, to be the highest in the treatment group III (0.15 mg\/kg\nconcentration) among the three treatment groups. These results are consistent\nwith the study by Shakeri and Boskabady, 2017.52<\/sup><\/p>\n\n\n\n

Because of their immunological importance, leukocytes (WBC) are\nhighly affected by inflammation and are more than usual in pathological cases.53<\/sup> Therefore, a\nrising count of WBCs in ethanol group II was gradually decreased when they were\ntreated in groups\nof 0.15, 0.30, and 0.45 mg\/kg concentration of aqueous extract of P. farcta<\/em>,\nwhich indicated two main factors: factors that have aided in the rise in the\nincidence of inflammation in the blood of experimental rats (ethanol), as seen\nin all experimental groups, Other factors have contributed to some extent to\nthe reduction of the incidence of ethanol-induced inflammation in groups III,\nIV, and V, which have been an aqueous extract of P. farcta<\/em> .54<\/sup> This shows\nthe WBC count in this group is closer to that in group I.<\/p>\n\n\n\n

The\neffect of P. farcta<\/em> extract on the GPx and MDA levels:<\/strong><\/p>\n\n\n\n

In the current investigation, oxidants and\nantioxidants were among the most crucial characteristics that were compared\nsince they are impacted by several physiological aspects brought on by the\naction of ethanol and the impact of P. farcta<\/em>. The treatment group with\nthe lowest concentration displayed the highest MDA value compared to all\nexperimental groups, including group II (ethanol). Specifically, the 0.30 and\n0.45 mg\/kg of aqueous extract of P. farcta<\/em> after receiving 0.005 ml\/g of\n35% ethanol had a noticeable effect in that it lowered the level of MDA to the\nlowest level in the IV and V groups.55<\/sup> The low\npercentage of MDA in the 0.30 and 0.45 mg\/kg of aqueous extract of P. farcta<\/em>\nafter receiving 0.005 ml\/g of 35% ethanol is explained by oxidants being\ninversely related to GPx levels.<\/p>\n\n\n\n

Oxidants and\nantioxidants are among the most critical parameters that were compared in the\ncurrent study because they are affected by the different physiological factors\nresulting from the action of ethanol and the effect of P. farcta.<\/em> MDA is\nproduced as a by-product that has the role of head of the oxidative reaction and\nis one of the vital signs of oxidative stress,56<\/sup> which occurs\ndue to the accumulation of free radicals that increase lipid oxidation as a\nresult of the imbalance between oxidizing substances and antioxidants, which\nleads to cell damage such as liver cells.57,58<\/sup> Therefore,\nits accumulation in the blood leads to excess free fatty acids and then\nhyperlipidemia, which can cause the overproduction of reactive oxygen species (ROS), thereby damaging the mitochondrial DNA.59<\/sup> MDA from\nlipid peroxide is associated with an intense contributory link due to the\npresence of two groups of carbonyl within the molecule, affecting its function.60<\/sup> So the low\nlevel of antioxidants such as SOD, GPx, glucose, or excessive output of ROS\nsuch as (OH-), superior (O2\u2212), and (H2O2) will both cause an increase in\noxidative stress, thereby increasing the level of MDA.61<\/sup>Themajor inflammatory factors are increased oxidative substances, oxidative\nstress, and ROS levels.62<\/sup> Increased\nlevels of ROS lead to the oxidation of polyunsaturated fatty acids (PUFA) found\nabundantly in cell membranes to form MDA. Hence the low production of SOD, GPx,\nand Catlaz. Under oxidative stress conditions, this MDA might be utilized as a\nbiomarker of the cell damage caused by free radicals,63<\/sup> Accordingly,\nit can be argued that the cellular machinery for reducing oxidative stress is\ndone by increasing antioxidants that interact with oxidants (free radicals and\ntheir types),64<\/sup> but this\nmechanism occurs within the low limits of fat oxidation by-products and cannot\ntreat the large quantities that occur to accumulate and cause cell aging and\nsome pathological conditions.65,66<\/sup><\/p>\n\n\n\n

Since the oxidants are inversely\nproportional to the levels of GPx, and this explains the low percentage of MDA\nin the groups treated with the aqueous extract of P. farcta<\/em>, the effect\nof the GPx is attributed to the presence of the\nflavonoids,9<\/sup> which are polyphenols that prevent the\noxidation reactions by giving free radicals one electron in exchange for a\nnon-double electron, therefore lowering their quantity.67<\/sup> Therefore, to\nmaintain normal metabolism in the body, GPx is an essential antioxidant. Some\nrecent studies suggest that glutathione types are associated with the\noccurrence, development, and treatment of different types of tumors.68<\/sup>and prevention.\nIn addition to being an antioxidant, GPx is an antioxidant, and it is vital to human health,\nreducing the generation of free radicals through their unique chemical reaction 69<\/sup> and\nneutralizing free radicals from their original form 57<\/sup>. For this\nreason, there are opposite results between MDA and GPx levels.70<\/sup><\/p>\n\n\n\n

Conclusions<\/strong><\/p>\n\n\n\n

It was found that the aqueous extract\nof the P. Farcta fruits had an apparent effect on reducing the inflammatory\nmarkers that were measured in laboratory albino rats, which included CRP,\nalbumin, GPx, MDA, and WBC because it contains antioxidants such as gallic\nacids and vanillic acids and reduces inflammation such as apigenin, quercetin,\nand luteolin.71,72<\/sup> Many types of flavonoids are\nanti-inflammatory agents that reduce CRP levels.73<\/sup> There was no apparent effect on the\nESR level in the treatment groups fed high concentrations of the aqueous\nextract of P. farcta<\/em>, which reduced the percentage of MDA.<\/p>\n\n\n\n

Acknowledgments<\/strong><\/p>\n\n\n\n

The authors would like to thank Dr. Ali Kareem Khudair (Dean of Nursing Faculty), Dr. Rasha A. Jawad (Physiologist), and Dr. Zaki Sabah Musaihib for their useful help in this work.<\/p>\n\n\n\n

Conflict of Interest<\/strong><\/p>\n\n\n\n

The authors declare that the research was conducted without any commercial or financial relationships that could be construed as a potential conflict of interest.<\/p>\n\n\n\n

Reference<\/strong><\/p>\n\n\n\n

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