Co esponding au ho : Jude Nnaemeka Okoyeh
Copy igh © 2025Au ho (s) e ain he copy igh o his a icle. This a icle is published unde he e ms o he C ea i e Commons A ibu ion License 4.0.
Hypolipidemic and an ioxidan e ec s o ui ex ac o Vi ex doniana (Black Plum) in
albino a s
Vic o ia Nonyelum Olli 1 and Jude Nnaemeka Okoyeh 2, *
1 Depa men o Pha macology and Toxicology, Chukwuemeka Odumegwu Ojukwu Uni e si y Igba iam campus Nige ia.
2 Depa men o Medical Labo a o y Science and Biology, School o Nu sing and Heal h Sciences, Neumann Uni e si y, One
Neumann D i e, As on, PA, 19014. USA.
Wo ld Jou nal o Ad anced Resea ch and Re iews, 2025, 26(01), 3732-3741
Publica ion his o y: Recei ed on 18 Ma ch 2025; e ised on 23 Ap il 2025; accep ed on 26 Ap il 2025
A icle DOI: h ps://doi.o g/10.30574/wja .2025.26.1.1480
Abs ac
In oduc ion: Hype lipidemia is a lipid me abolic diso de and he majo isk ac o o he de elopmen o
ca dio ascula diseases (CVDs). Because mos o he cu en hypolipidemic d ugs a e expensi e wi h po en ial side
e ec s, he esea ch ocusing on na u al al e na i e medicines is ele an . The ui ex ac o Vi ex doniana is used by
some adi ional medicine p ac i ione s in Nige ia o ea CVDs. This s udy is aimed a in es iga ing he hypolipidemic
and an ioxidan e ec s o e hanol ui ex ac o V. doniana in high- a die (HFD) induced in albino a s. O al
adminis a ion o ex ac a 250, 500 and 1000 mg/kg body weigh on HFD induced hype lipidemia las ed o 28 days.
A o as a in (1.2 mg/kg) se ed as s anda d d ug. Hypolipidemic e ec was checked by he measu emen o se um lipid
p o ile and e ec on oxida i e s ess.
Resul s: The esul s e ealed a dose dependen signi ican (P<0.05) dec ease in malondialdehyde (MDA), inc ease in
supe oxide dismu ase (SOD) and ca alase (CAT) le els when compa ed o he nega i e con ol. This a es s o he abili y
o he ex ac o boas he an ioxidan de ence mechanism in he animals. Posi i e e ec on CVDs was u he con i med
by he obse ed dose ela ed signi ican (p<0.05) educ ion in se um lipids ( o al choles e ol, o al glyce ides and low
densi y lipop o ein) p o ile o he ea ed a s when compa ed o he nega i e con ol.
Conclusion: The ui ex ac o V. doniana possesses se um lipid lowe ing e ec s; i s olklo ic use in he ea men o
ca dio ascula diseases could he e o e be jus i ied. Fu he s udies need o ocus on he isola ion and cha ac e iza ion
o he seconda y me aboli es esponsible o his obse ed ac i i y.
Keywo ds: Hype lipidemia; Hypolipidemia; Ca dio ascula diseases; A he oscle osis
1. In oduc ion
The global bu den o disease has d ama ically shi ed om communicable diseases o non-communicable diseases
including ca dio ascula diseases (CVDs), cance and diges i e diseases. This is expec ed o inc ease o 59% [1].
Ca dio ascula diseases accoun o mos non communicable disease dea hs and is esponsible o o e 17.3 million
dea hs pe annum [2].
Li e p oduces choles e ol and expo s i o o he pa s o he body o he p oduc ion o ho mones and cell memb anes.
Accele a ed deposi ion o choles e ol in he inne walls o a e ies leads o a he oscle osis which is he unde lying cause
o ca dio ascula disease. A he oscle osis is linked o high le els o choles e ol in he blood, pa icula ly o high le els
o low-densi y lipop o ein (LDL)-bound choles e ol which is o he wise known as he ‘‘bad choles e ol’’[3]. Fu he mo e,
he e is a nega i e co ela ion be ween high-densi y lipop o ein (HDL) le els, he ‘‘good choles e ol’’ and a e ial
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disease [3]. Hype lipidemia is a highly p edic i e isk ac o o a he oscle osis, co ona y a e y and ce eb al ascula
diseases. I is cha ac e ized by ele a ed se um o al choles e ol and e y LDL choles e ol and dec eased HDL le els [4].
High- a die (HFD) is a majo cause o obesi y. Excess calo ies in he body a e con e ed o iglyce ides which a e
mainly s o ed in he adipose issues [5]. High iglyce ide le el inc eases he isk o a he oscle o ic CVD [6].
The mode n allopa hic d ugs used o he ea men o hype lipidemia a e e ec i e, bu a e expensi e and associa ed
wi h side-e ec s leading o pa ien incompliance [7]. Medicinal plan s a e he oldes known na u al sou ce o medicine
wi h li le o no side e ec s. Many plan species such as Vi ex doniana ui s ex ac ha e been used in adi ional
medicine o ea hype lipidemia. In Nige ia, Vi ex doniana ui is commonly e e ed o as Black Plum. Black plum is
known as O i i (Yo uba), Mbembe (Igbo) and Dinyan (Hausa). The u al people o Nige ia consume he ma u ed ui
pulp mainly as a snack and o i s belie ed seda i e e ec s. This s udy in es iga es he hypolipidemic and an ioxidan
p ope ies o e hanol ex ac o Vi ex doniana ui in HFD induced hype lipidemia in albino a s.
Figu e 1 F esh ui s and lea es o Vi ex doniana
2. Ma e ial and me hods
2.1. Plan ma e ials
2.1.1. Sample collec ion and Iden i ica ion
The esh ui s o Vi ex doniana we e pu chased om Ekwulobia in Anamb a s a e o Nige ia. The ui was
au hen ica ed by a Taxonomis a he depa men o Bo any, Nnamdi Azikiwe Uni e si y, Awka, Nige ia, and a ouche
specimen numbe (NAUBT 3218) was assigned o i .
2.1.2. Chemicals, eagen s and d ugs:
A o as a in,( (Lipi o by P ize , Uni ed s a es o Ame ica), 96 % / e hanol analy ical g ade (Zigma, India), chlo o o m
(Zigma, India), Elisa eagen s (Ha man Finochem Limi ed India).
2.1.3. High a eed ma e ials
G owe eed (Top Feed P emie Feed Mills Sapele, Del a s a e, Nige ia), egg yolk, c ay ish, Palm ke nel cake (P.K.C) and
Ma ga ine
2.1.4. Animals
Thi y albino a s (130-150 g) o bo h sexes we e pu chased om he labo a o y animal house o he Depa men o
Pha macology and Toxicology, Chukwuemeka Odumegwu Ojukwu Uni e si y Igba iam campus Anamb a s a e Nige ia,
we e used o he s udy. The a s we e housed in clean plas ic cages, supplied wi h clean d inking wa e and ed wi h
G owe eed (Top Feed P emie Feed Mills Sapele, Del a s a e, Nige ia). E hical app o al numbe
PHACOOU/AREC/2023/033 was assigned o a es he animals we e ca ed o acco ding o he Facul y o Pha macy
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(COOU) Animal Resea ch E hics Commi ee guidelines (PHACOOUAREC), which a e in line wi h he Na ional Ins i u e
o Heal h (NIH), USA, guidelines o he ca e and use o labo a o y animals.
2.1.5. Dosage selec ion
Dose o ex ac adminis e ed o animals we e 1/20 h, 1/10 h and 1/5 h o he es ima ed LD50 [8] and he ui ex ac
was adminis e ed o ally.
2.1.6. Fo mula ion o he high a eed
The mix u e o ollowing ing edien s in hei a ious p opo ion we e used o ed he animals; 35% Top Feed, 10% egg
yolk, 5% c ay ish, 35% Palm ke nel cake (P.K.C) and 15% ma ga ine. he eeding las ed o ou weeks [9].
2.2. Ex ac ion o plan ma e ial
Ex ac ion was done using a me hod desc ibed by [10]. The ui s we e cleaned o emo e sand and o he deb is. A e
emo ing he hin me ica p, he leshy juicy mesoca p was sc aped o om he seeds and d ied o a pe iod o wo
weeks unde oom empe a u e. This d ied mesoca p was g inded in o powde wi h he help o an elec ical g inde .
Abou , 800 g o he powde ed ma e ial was cold mace a ed in 80 % e hanol. The mix u e was agi a ed in e mi en ly
o h ee days (72 hou s). The il a e was eco e ed and concen a ed o d yness using wa e ba h a 40 OC. The
pe cen age yield o he ex ac was calcula ed and he ex ac s o ed in a e ige a o un il when needed.
2.3. Quali a i e phy ochemical analysis
Sc eening o he p esence o seconda y me aboli es was ca ied ou ollowing he phy ochemical es s as demons a ed
by [11]. The ollowing seconda y me aboli es we e es ed o : annins, alkaloids, educing suga s, la onoids, glycosides,
an h aquinones, saponins, acidic compounds and p o eins.
2.4. Acu e oxici y s udy
The oxici y es was conduc ed using he up and down p ocedu e (UDP) adop ed by [12] and e ised by [13]. Using his
me hod, he animals we e dosed one a a ime and he doses we e dependen on he esponse o he i s animal o he
ini ial dose. The second animal ecei es a lowe dose i he i s animal dies ( he ini ial dose is dec eased by a ac o o
3.2) o he second animal ecei es a highe dose i he i s animal su i es ( he ini ial dose is inc eased by a ac o o
3.2). Th ee albino a s (130-150 g) we e used as s a ing poin . Two a s se ed as nega i e con ol ha ing ecei ed 10
ml/kg o dis illed wa e o ally while he es animal ecei ed a de aul o al dose o 5000 mg/kg o he ex ac . The
animals we e hen obse ed con inuously o 4 hou s o changes in beha iou and o any o he ob ious signs o
oxici y and subsequen ly daily o a o al o 14 days o delayed oxici y
2.5. Induc ion o hype lipidemia
Hype lipidemia was induced by eeding he animals on high a die composed o 35 % Top g owe eed, 10 % egg yolk,
5 % c ay ish, 35 % Palm ke nel cake (P.K.C) and 15 % Ma ga ine o wo weeks [9]. The ea men pa e n was as seen
s a ed below:
• G oup 1: No mal con ol (NC)
• G oup 2: Nega i e con ol (NEG.C)
• G oup 3: Posi i e con ol (1.2 mg/kg A o as a in)
• G oup 4: 250 mg/kg ex ac + High a eed
• G oup 5: 500 mg/kg ex ac + High a eed
• G oup 6: 1000 mg/kg ex ac + High a eed
All he g oups we e ea ed wi h he ex ac excep he nega i e con ol g oup. In he same manne all he g oups we e
ea ed wi h high a die (induc ion o hype lipidemia) excep he no mal con ol g oup.
Bo h he s anda d A o as a in and ui ex ac we e adminis e ed o ally once daily o 28 days. On he 28 h day, he
animals we e as ed o e nigh and we e humanely sac i iced wi h excess chlo o o m. The blood sample we e collec ed
o biochemical es s while he li e was ha es ed o his opa hological examina ion.
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2.5.1. Biochemical assays
De e mina ion o se um o al choles e ol:
Se um o al choles e ol (TC) was e alua ed using Randox comme cial assay ki s, applying he me hods desc ibed by
[14]. One millili e (1ml) o he wo king Choles e ol eagen (1ml) was added in o ubes labelled blank, s anda d and
es g oups. Ten mic oli es o s anda d choles e ol eagen , and samples we e added in o hei espec i e ubes. They
we e mixed and allowed o s and o 10 minu es a oom empe a u e. Abso bance o samples and s anda d we e ead
wi h he aid o a spec opho ome e a 500 nm. To al choles e ol le el in sample was calcula ed using he o mula
To al choles e ol in sample (mg/dl) = x Concen a ion o s anda d.
De e mina ion o se um iglyce ide
Se um iglyce ide was e alua ed acco ding o he me hods desc ibed by [15]. One millili e (1 ml) o he wo king
iglyce ide eagen was added in o ubes labeled blank, s anda d and es g oups. Ten mic oli es o s anda d
iglyce ide eagen , and samples we e added in o hei espec i e ubes. They we e mixed and allowed o s and o 10
minu es a oom empe a u e. Abso bance o samples and s anda d we e ead wi h he aid o a spec opho ome e a
500 nm. To al choles e ol le el in sample was calcula ed using he o mula;
To al iglyce ide in sample (mg/dL) = x Concen a ion o s anda d
De e mina ion o se um high densi y lipop o ein choles e ol (HDL-choles e ol):
Se um HDL-choles e ol was e alua ed acco ding o he me hods de eloped by Na ional Ins i u e o Heal h Consensus
De elopmen Con e ence S a emen . One hund ed mic oli es (100 ul) o samples and s anda d choles e ol eagen
we e dispensed in o es ubes con aining 250 ul o HDL choles e ol p ecipi a e (R1). The mix u e was cen i uged a
4000 pm o 10 minu es. The ea e , 100 uL o samples and s anda d supe na an s we e added o ano he se o es
ubes labeled samples and s anda d con aining choles e ol eagen . The mix u e was incuba ed o 10 minu es a oom
empe a u e and abso bance o s anda d and samples we e measu ed agains eagen blank a 500 nm wi hin 60
minu es using Spec opho ome e . HDL-choles e ol le el in sample was calcula ed using he o mula below;
HDL choles e ol in sample (mg/dL) = x Concen a ion o s anda d.
De e mina ion o se um low densi y lipop o ein choles e ol (LDL-choles e ol):
Low densi y lipop o eins (LDL) choles e ol in se um was calcula ed using he equa ion desc ibed by [16]. The
F iedewald’s equa ion es ima es he alue o HDL-C using he alues o o al choles e ol, iglyce ide and HDL-
choles e ol. [16].
LDL choles e ol (mg/dl) = To al choles e ol - - HDL choles e ol.
2.5.2. E ec o he ex ac on oxida i e s ess
De e mina ion o plasma Thioba bi u ic acid:
Thioba bi u ic acid eac i e subs ances (TBARS) assay is an es ablished me hod o quan i ying lipid pe oxides. Lipid
pe oxida ion gene a es pe oxide in e media es which upon clea age eleases malondialdehyde, a p oduc which eac s
wi h hioba bi u ic acid [17]. The ac i i y o TBARS was de e mined by he me hods o [18].
Assay o an ioxidan ac i i y o supe oxide dismu ase (SOD):
The ac i i y o supe oxide dismu ase (SOD) was de e mined using se um om he expe imen al a s. The ac i i y o
supe oxide dismu ase was assessed using he NWLSSTM, supe oxide ac i i y assay. The me hod was based on
moni o ing he au o-oxida ion a e o haema oxylin as desc ibed by [19]. The sample’s SOD ac i i y was de e mined by
measu ing he a io o au o-oxida ion a e in he p esence and absence o he sample and exp essed as adi ional
‘McCo d-F ido ich.
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Assay o an ioxidan ac i i y o ca alase (CAT)
The ca alase ac i i y o he hemolysa e (a solu ion o lysed ed blood cells) was de e mined by adop ing he me hod o
[20]. The assay is based on he disappea ance o H202 in he p esence o he enzyme sou ce a 26 0C. In b ie , he
hemolysa e was p epa ed om lysed RBC suspension and u he dilu ed using phospha e bu e (pH 7.0). The eac ion
mix u e con aining 0.05 M phospha e bu e (pH 7.0), 1.2 mM H202 and 0.2 ml o dilu ed hemolysa e was allowed o
s and o 25 minu es. A he end o 25 minu es he eac ion was s opped by he addi ion o 2.5 ml o pe oxidase eagen
con aining pe oxidase and he ch omogen sys em. Pe oxidase educed he H202 o gi e a ed colo ed compound and
abso bance was measu ed a 505 nm. Wi h each assay a sui able blank which con ained he phospha e bu e o
main ain he pH o he mix u e, hyd ogen pe oxide which is same concen a ion as he es sample and dis illed wa e
ins ead o he hemolysa e and a con ol which con ained l ml sodium azide, a ca alase inhibi o was p o ided.
2.5.3. De e mina ion o body mass
The animals we e weighed a he beginning o he expe imen and hen weekly o ou weeks. Weigh s gained by he
a s we e calcula ed as he di e ence be ween ini ial and inal weigh s and he esul s we e p esen ed as a pe cen age
o he ini ial weigh s.
2.6. S a is ical analysis
Da a ob ained om he s udy was analyzed using S a is ical Package o Social Sciences (SPSS-25). Resul s we e
p esen ed as mean ± S anda d e o o mean (SEM) o sample eplica es. Raw da a was subjec ed o one-way analyses
o a iance (ANOVA) ollowed by pos hoc u key’s es . p<0.05 was conside ed o be s a is ically signi ican .
3. Resul s
3.1. Yield o ex ac
The weigh o he V. doniana ui s a e he emo al o he seeds was 765 g and he c ude ex ac ob ained om i was
333 g. The pe cen age yield was 43.8%
3.2. Acu e Toxici y es (LD50) o he ex ac
O al adminis a ion o he ui ex ac up o 5000 mg/kgbw dose p oduced no change in beha iou , nei he was he e
any mo ali y in any o he g oups. The e o e, he LD50 o e hanol ui ex ac o Ve ex doniana was abo e 5000
mg/kgbw.
3.3. Phy ochemical sc eening o he ex ac
Phy ochemical analysis o he ex ac e ealed he abundance p esence o anins, la onoids, glycosides, saponins,
s e oids, an h aquinones, and ca bohyd a es while alkaloids, and educing suga s we e in mode a e p esence (Table
1).
Table 1 Phy ochemical sc eening o he ex ac
Cons i uen
Alk
Tan
Fla
Gly
Sap
An h
S e
Ca b
Acid cpds
Red suga
P esence
++
+++
+++
+++
+++
+++
+++
++
+++
++
Key: Alk = alkaloids, Tan= annins, Fla = la onoids, Gly= glycosides, An h = an h aquinones, Sap=saponin, S e= s e oids, Ca b = ca bohyd a es, Red
suga = educing suga , (++) = mode a ely p esen , (+++) = abundance
3.4. E ec o ex ac on se um lipid p o ile
The ui ex ac caused a dose ela ed signi ican (P<0.05) dec ease in TC ( o al choles e ol), TG ( o al glyce ides), LDL
(low densi y lipop o ein) and inc ease in HDL (high densi y lipop o ein) when compa ed o he nega i e con ol (Figu e
2)
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Key: TC= To al Choles e ol, TG= T iglyce ides, HDL-C= High densi y lipop o eins, LDL-C= Low densi y lipop o eins, NC= No mal con ol, and H2o=
Nega i e con ol
Figu e 2 E ec o e hanol ui ex ac o Vi ex doniana on se um lipid p o ile
3.5. E ec s o ex ac on oxida i e s ess pa ame e s
Key: MDA= Malondiadehyde, SOD=supe oxide dismu ase, CAT =ca alase ac i i y, NC= No mal con ol, and H2o= wa e
Figu e 3 E ec o e hanol ui ex ac o Vi ex doniana on oxida i e s ess pa ame e s
The ex ac caused a dose dependen signi ican (P<0.05) dec ease in malondialdehyde (MDA), (a p oduc o lipid
oxida ion), inc ease in supe oxide dismu ase (SOD) which neu alizes ee adical, and inc ease in ca alase (CAT) which
p o ec s cells om oxida i e damage when compa ed o he nega i e con ol g oup (Figu e 3)
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3.6. E ec o ex ac on body weigh
Conside ing he weigh a e induc ion(WAI) o hype lipidaemia and weigh a e 28 days ea men (WAT), he ex ac
caused a dose ela ed signi ican (P<0.05) dec ease in weigh s o he animals in he ea ed g oups when compa ed he
ini ial weigh a e induc ion in all he g oups.
Key: WBI= weigh be o e induc ion, WAI= weigh a e induc ion, WAT=weigh a e ea men , NC= no mal con ol, and H2o= wa e
Figu e 4 E ec he ex ac on body weigh
4. Discussion
Choles e ol is a i al pa o all cell memb ane and i is essen ial molecule o all li ing beings [21]. La ge amoun o
choles e ol is ound in b eas milk, whe e i plays pa in in an nou ishmen and b ain de elopmen [22]. I helps in he
healing and epai o blood essels [23]. Howe e , he ccele a ed deposi ion o choles e ol in he inne walls o a e ies
leads o a he oscle osis, he unde lying cause o ca dio ascula disease. A he oscle osis is linked o high le els o
choles e ol in he blood, pa icula ly, he low-densi y lipop o ein bound choles e ol (LDL-C) he ‘‘bad choles e ol’’ [3].
A o as a in dec eases he amoun o LDL-C in he blood he eby p e en ing he e en s associa ed wi h ca dio ascula
disease [24]. I does his by ac ing as a compe i i e inhibi o o 3-hyd oxy-3-me hylglu a yl-coenzyme A (HMG-CoA)
educ ase, he enzyme in ol ed in hepa ic choles e ol biosyn hesis.
High se um le els o TC and LDL a e associa ed wi h an inc eased isk o a he oscle osis [25]. The ea men wi h he
ui ex ac o V. doniana o 28 days, caused a dose dependen signi ican (P<0.05) educ ion in TC, TG, LDL as well as
a dose dependen signi ican (P<0.05) inc ease in HDL. Hype choles e olemia and hype iglyce idemia a e
independen isk ac o s ha alone o oge he can accele a e he de elopmen o co ona y a e y disease and he
p og ession o a he oscle o ic lesions [26]. Ami khizi [27] demons a ed inc ease in he bioa ailabili y o ee a y
acids can inc ease lipid pe oxida ion. In his s udy, he ac ha his ui ex ac was able o cause a dec ease in TC, TG
LDL and an inc ease in HDL concen a ions sugges s he ui o Vi ex doniana may play a p o ec i e ole agains
hype lipidemia.
Oxida i e s ess occu s when he e is an imbalance be ween eac i e oxygen species (ROS), ee adicals and hei
sca enging by he na u al an ioxidan sys em [28]. Oxida i e s ess is associa ed wi h hype lipidemia, which accele a es
a he oscle osis [29]. High a die (HFD) can led o an inc ease in ee adical p oduc ion in i o, ollowed by oxida i e
s ess [30]. The adminis a ion o he ex ac caused inc eased ac i i y o he an ioxidan de ense sys em in he ea ed
g oups in a dose dependen manne . This was e ealed by he obse ed dose-dependen signi ican (P<0.05) inc ease
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in SOD and CAT le els and educ ion in he MDA le el. Ca alase(CAT) is an enzyme ound in ed blood cells ha b eaks
down he ee adical hyd ogen pe oxide (H2O2) in o wa e and oxygen. This obse ed an ioxidan p ope y o Vi ex
doniana ui ex ac con i ms he epo by [31][32]. An ioxidan s ha e he po en ials o posi i ely a ec
hype lipidemia by educing oxida i e s ess, which is a key con ibu o o he de elopmen o he hype lipidemia by
neu alizing ee adicals. (h ps://www.na u e.com). These esul a es he abili y o his ui ex ac o educe
oxida i e s ess which may ha e con ibu ed o i s hypolipidemic e ec since obesi y has been ound o be an
independen isk ac o o inc easing lipid pe oxida ion and dec eased ac i i y o cy op o ec i e enzymes [33].
The quali a i e phy ochemical sc eening o he ui ex ac e ealed he abundance o seconda y me aboli es like
la onoids, an h aquinone, and annins. The an ioxidan and hypolipidemic ac i i ies o an h aquinones and la onoids
ha e p e iously been epo ed [34] [35]. Hence, he hypolipidemic and an ioxidan ac i i ies exhibi ed by V. doniana
ui ex ac could be a ibu ed o he syne gis ic ac ion o he bioac i e compounds p esen in i .
5. Conclusion
The ui ex ac o V. doniana possesses se um lipid lowe ing e ec s, i s olklo ic use in he ea men o ca dio ascula
disease could he e o e be jus i ied. We sugges ha u he s udies should include he isola ion o he seconda y
me aboli es esponsible o hese obse ed ac i i ies.
Compliance wi h e hical s anda ds
Disclosu e o con lic o in e es
The au ho s wish o con i m ha he e is no known con lic o in e es s associa ed wi h his pape and he e has been
no signi ican inancial suppo o his wo k ha could ha e in luenced i s ou come.
S a emen o e hical app o al
E hical app o al numbe PHACOOU/AREC/2023/033 was assigned o a es he animals we e ca ed o acco ding o
he Facul y o Pha macy (COOU) Animal Resea ch E hics Commi ee guidelines (PHACOOUAREC), which a e in line wi h
he Na ional Ins i u e o Heal h (NIH), USA, guidelines o he ca e and use o labo a o y animals.
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