Co esponding au ho : Mbagwu Ikechukwu Sonne.
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Inhibi ion o ad anced glyca ion end p oduc and lipid pe oxida ion by ex ac and
ac ions o Newbouldia lae is
Daniel Lo anna Ajaghaku 1, Ikechukwu Sonne Mbagwu 2, *, and Ama a Anwuchaepe Ajaghaku 3, 4
1 Depa men o Pha macology, Facul y o Pha maceu ical Sciences, Enugu S a e Uni e si y o Science and Technology,
Enugu S a e, Nige ia.
2 Depa men o Pha macology and Toxicology, Facul y o Pha maceu ical Sciences, Nnamdi Azikiwe Uni e si y Agulu,
Anamb a S a e, Nige ia.
3 Depa men o Pha macognosy and T adi ional Medicine, Facul y o Pha maceu ical Sciences, Da id Umahi Fede al
Uni e si y o Heal h Sciences, Ubu u, Ebonyi S a e, Nige ia.
4 In e na ional Ins i u e o Pha maceu ical Resea ch and Inno a ion, Da id Umahi Fede al Uni e si y o Heal h Sciences,
Ubu u, Ebonyi S a e, Nige ia.
Wo ld Jou nal o Ad anced Resea ch and Re iews, 2025, 26(02), 2514-2530
Publica ion his o y: Recei ed on 02 Ap il 2025; e ised on 10 May 2025; accep ed on 12 May 2025
A icle DOI: h ps://doi.o g/10.30574/wja .2025.26.2.1836
Abs ac
Newbouldia lae is is gene ally known o i s signi ican an idiabe ic po en ials. Ad anced glyca ion end-p oduc s (AGEs)
and lipid pe oxida ion con ibu e signi ican ly o he pa hogenesis o diabe ic complica ions h ough oxida i e s ess
and p o ein damage. This s udy e alua ed he inhibi o y e ec s o ex ac and ac ions o Newbouldia lae is lea es on
AGE o ma ion and lipid pe oxida ion. The lea es we e ex ac ed using 70% aqueous e hanol and pa i ioned in o n-
hexane, e hyl ace a e, bu anol, and wa e ac ions. In i o assays e ealed he e hyl ace a e ac ion wi h he highes
o al phenolic con en and exhibi ed he s onges e ic educing an ioxidan powe and inhibi ion o lipid pe oxida ion.
The o ma ion o AGEs and glyca ion-induced p o ein ca bonyla ion we e signi ican ly supp essed in a concen a ion-
dependen manne , wi h he e hyl ace a e ac ion demons a ing he mos po en ac i i y in weeks 2 – 4 a 0.4 – 1.6
mg/ml concen a ions, compa able o aminoguanidine, a s anda d AGE inhibi o . The bu anol and wa e ac ions also
showed no able inhibi o y e ec s, whe eas he n-hexane ac ion exhibi ed he leas ac i i y. The inhibi o y po en ial o
he ac ions co ela ed wi h hei phenolic con en , sugges ing a phenol-media ed mechanism. These indings suppo
he he apeu ic po en ial o N. lae is, pa icula ly i s phenol- ich ac ions, in mi iga ing oxida i e s ess and p o ein
glyca ion associa ed wi h diabe es melli us and i s complica ions.
Keywo ds: Newbouldia Lae is; Ad anced Glyca ion End-P oduc s (Ages); Lipid Pe oxida ion; Diabe ic Complica ions;
Phenolic Compounds; An ioxidan Ac i i y
1. In oduc ion
Diabe es melli us is a me abolic condi ion ma ked by hype glycemia [1]. Long e m exposu e o high glucose
concen a ion in he blood is associa ed wi h nume ous complica ions ha lead o impai men o kidney, eyes, ne es
and blood essels s uc u es and unc ions. These complica ions ep esen majo cause o mo bidi y and mo ali y
associa ed wi h diabe es [2]. One o he majo pa hways in ol ed in he de elopmen and p og ession o di e en
diabe ic complica ions is p o ein glyca ion eac ion leading o he o ma ion o ad anced glyca ion end p oduc s [3].
Some o he diabe ic complica ions associa ed wi h his p ocess include bu no limi ed o neph opa hy, e inopa hy and
neu opa hy [4]. O he consequences o ad anced glyca ion end p oduc s (AGEs) include ca dio ascula complica ions,
neu odegene a i e de angemen , bone diso de s and e ec ile dys unc ion o men ion bu a ew [5].
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Ad anced glyca ion end-p oduc s a e he inal p oduc s o he non-enzyma ic eac ion be ween educing suga and
amino g oups in p o eins, lipop o eins and nucleic acids [6]. Du ing sus ained hype glycemia, glucose c ea es co alen
adduc s wi h amino acid esidues in p o eins, which ini ia es his p ocess. This p ocess o p o ein glyca ion induces
con o ma ional changes ha a ec s he s uc u al and unc ional ac i i ies o p o eins including hei abili y o ac as
ecep o s o ligand/d ug in e ac ion as well as hei me abolic unc ions [7].
The pa hological implica ions o AGEs a e asc ibed o hei abili y o p oduce eac i e oxygen and ni ogen species as
well as oxida i e s ess and in lamma o y condi ions ha lead o s uc u al and unc ional p o ein al e a ion, cellula
dys unc ion and o he issue and o gan damages [8]. The ee adicals gene a ed h ough a ious glyca ion s eps and
o he hype glycaemic media ed p ocesses also p oduce lipid pe oxida ion wi h i s associa ed eac i e ca bonyl
p oduc s [9]. The lipid pe oxida ion eac i e p oduc s ac as bo h p ecu so o AGEs o ma ion and as di ec p o ein
damage ini ia o he eby ampli ying he hype glycaemia media ed p o ein damage [5]. The inhibi ion o ad anced
glyca ion end p oduc s ad lipid pe oxida ion he e o e ep esen s an impo an pha macological a ge o he
p e en ion o mi iga ion o li e h ea ening complica ions o diabe es.
Fo many decades, na u al p oduc s ha e been used as a sou ce o he apeu ic agen s because o he exis ence o a ious
bioac i e compounds and hey a e belie ed o be non- oxic o a la ge ex en [10]. Newbouldia lae is commonly e e ed
o as he A ican Bo de T ee o Bounda y T ee can be seen g owing in opical ain- o es egions and has been used
o many yea s in he p ac ice o adi ional medicine. This plan is also ich in many phy ochemical cons i uen s and
seconda y me aboli es including Alkaloids, Fla onoids, Saponins, Tannins, Glycosides Phenols and he i amins A, B1,
B2, B6, B12, C, D, E and K which a e e hno-pha macologically signi ican [11]. N. lae is also exhibi an i-in lamma ion,
an ihype ensi e, an icoagulan , an ibac e ial, and an ioxidan p ope ies which a e comp ehensi ely epo ed in he
cu en li e a u e [12]. Newbouldia lae is has been shown in ecen esea ch o ha e an idiabe ic po en ial, wi h
hypoglycemia e ec s simila o hose o glibenclamide [13, 14]. In ype 2 diabe es animals, he bu anol ac ion
imp o ed insulin sec e ion, lipid p o ile, and glucose/ a ole ance while signi ican ly lowe ing blood glucose, body
weigh , and insulin esis ance [15]. Addi ionally, he plan has also been epo ed o exe i ’s an idiabe ic e ec s by
lowe ing oxida i e s ess and dec easing he abso p ion o glucose, which a ec s insulin sensi i i y and panc ea ic β-
cell ac i i y [16]. In addi ion, Newboulasides A and B, wo no el ca eic acid glycosides disco e ed om N. lae is,
demons a ed po en α-amylase inhibi ion [17], indica ing ha enzyme inhibi ion is a c ucial mechanism. These indings
suppo i s long-s anding use in he ea men o diabe es. This s udy seeks o in es iga e u he he apeu ic po en ials
o N. lae is in he p e en ion and managemen o diabe es complica ions.
2. Ma e ials and Me hods
2.1. Plan ma e ial
Newbouldia lae is lea es we e collec ed in Oba, Enugu S a e, Nige ia, and con i med by a ained axonomis , M . Felix
Nwa o om he Depa men o Pha macognosy and En i onmen al Medcine, Uni e si y o Nige ia Nsukka, Enugu
S a e, Nige ia. The plan ma e ial was ai d ied and c ushed o powde . The ouche specimen was placed in he
he ba ium o he Facul y o Pha maceu ical Science a Nnamdi Azikiwe Uni e si y's Agulu Campus (PCG 474/A/035).
2.2. Ex ac ion
A 2.5 kg quan i y o pul e ized lea es o N. lae is was cold mace a ed in 10 L o aqueous e hanol (70%) o 72 h wi h
in e mi en shaking. The esul ing solu ion was il e ed, and he il a e was p e-concen a ed in acuo using a o a y
e apo a o a 40°C and he ea e , d ied o a cons an weigh using an open wa e ba h a he same 40°C o ob ain he
e hanol ex ac .
2.3. F ac iona ion (Liquid-liquid Ch oma og aphy)
The e hanol ex ac (112 g) was dissol ed in dis illed wa e and subjec ed o liquid–liquid pa i ion successi ely wi h
2.5 L o n-hexane, e hyl ace a e, and hen bu anol using sepa a ing unnel o ob ain he n-hexane, e hyl ace a e and
bu anol soluble ac ions, espec i ely. The le o e po ion a e pa i ioning was used as he wa e ac ion. The
ac ions we e p e-concen a ed using o a y e apo a o a 40oC and d ied using wa e ba h a 40oC. The wa e ac ion
was eeze d ied.
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2.4. In i o analysis
2.4.1. To al phenolic con en o he ex ac and ac ions by Folin ciocal eu’s assay
The o al phenolic con en o he ac ions we e de e mined using he me hod desc ibed by Kim e al. [18]. One millili e
o he ex ac s (100 µg/ml) was mixed wi h 0.2 ml o Folin-Ciocal eu’s phenol eagen . A e 5 minu es, 1 ml o 7.6%
Na2CO3 solu ion was added o he mix u e ollowed by he addi ion o 2 ml o dis illed wa e . The mix u e (in duplica e)
was incuba ed a 40 °C o 30 minu es, a e which he abso bance we e ead a 760 nm using UV-VIS
spec opho ome e agains blank (con aining e e y o he componen o he mix u e excep sample). The o al phenolic
con en was es ima ed om he calib a ed cu e which was made by p epa ing gallic acid solu ion and exp essed as
millig ams o gallic acid equi alen (GAE) pe g am o he ex ac s.
2.4.2. Fe ic educing an ioxidan powe assay
The FRAP assay was conduc ed acco ding o he me hod epo ed by Benzie and S ain, [19]. FRAP eagen was eshly
made by mixing h ee solu ions a, b and c, 300 mM sodium ace a e bu e , pH = 3.6 (solu ion a), 10 mM 2,4,6- is(2-
py idyl)-s- iazine (TPTZ) solu ion in 40 mM HCl solu ion (b) and 20 mM e ic chlo ide (FeCl3) solu ion (c) in
p opo ions o 10:1:1 ( / / ). The eac ion was comple ed by keeping he eagen in da kness o 30 minu es. In he
es , 0.1 mL o ac ions and posi i e con ol asco bic acid (100, 200, 400, 800, and 1600 µg/mL) and FeSO4 (200, 400,
600, 800, and 1000 µM) we e mixed wi h 2.9 mL o FRAP eagen indi idually. An equal amoun o 5% Tween 80 (0.1
mL) was used as a blank (con ol). All samples we e p epa ed in iplica e and o exed o 1 minu e be o e being
incuba ed in he da k a 37 °C o 30 minu es. Each sample's ise in abso bance was e alua ed using a UV-Visible
spec opho ome e a 593 nm. The esul s we e compa ed wi h asco bic acid as posi i e con ol and FeSO4 was used
o calib a ion. FRAP ac i i y was es ima ed using e ous equi alen (FE) in µM.
2.4.3. Linoleic acid pe oxida ion assay
The p ocedu e was pe o med acco ding o modi ied me hod o Choi e al. [20]. The ac ions we e mixed wi h 550 μL
linoleic acid solu ion (0.28 mg linoleic acid and 0.28 mg Tween-20 in 100 μM phospha e bu e ,pH 7.4) a a ious
concen a ions (100 – 1600 μg/mL), 500 μL o phospha e bu e (100 μM, pH 7.4) and 150 μl o asco bic acid (10 μM).
Same concen a ions o T olox whe e used as e e ence s anda d while he blank con ained he ehicle (5% Tween 80)
in place o sample/s anda d. The linoleic acid pe oxida ion was ini ia ed by he addi ion o 0.1 mL FeSO4 (10 μM) and
incuba ed a 37°C o 60 min. The eac ion mix u e was cooled and 1.5 mL o ichlo oace ic acid (10% in 0.5% HCl)
added. Then, 3 mL TBA (1%, in 50 mM NaOH) was added. The eac ion mix u e and TBA solu ion we e hea ed in he
wa e ba h a 90oC o 60 min. A e cooling, 2 mL po ions we e aken om each sample and o exed wi h 2 mL
bu anol and cen i uged a 1000 x g o 30 min. The uppe laye o he esul ing solu ion was sepa a ed o
spec opho ome ic measu emen . The abso bance o solu ion was ead a 532 nm and calcula ed he pe cen age o
linoleic acid pe oxida ion inhibi ion in he ollowing equa ion:
Linoleic acid pe oxida ion inhibi ion (%) = ((Acon ol-Asample)/ Acon ol) x100
2.4.4. In i o glyca ion o bo ine se um albumin
The glyca ed BSA o ma ion was de e mined acco ding o a p e iously desc ibed me hod (Adisakwa ana e al. [21]
wi h sligh modi ica ion. Bo ine se um albumin (BSA) was used as he model p o ein in a concen a ion o 40 mg/ml
co esponding o physiological albumin concen a ion in human blood; simila ly, glucose (0.5 M) was used as he
glyca ing agen . B ie ly, BSA (40 mg/ml) was incuba ed wi h 0.5 M glucose in 0.1 M phospha e bu e saline (PBS) (pH
7.4), con aining 0.02 % sodium azide in he da k a 37 °C o 1, 2, 3, and 4 weeks. The solu ion con aining N. lae is
ac ions (0.1–1.6 mg/ml) dissol ed in PBS was added o he mix u es, be o e incuba ion. All incuba ions we e
pe o med unde s e ile condi ions. A small d op o chlo o o m was added o he solu ion and he co ks mois ened wi h
oluene o inhibi bac e ial g ow h. Fluo escen in ensi y a an exci a ion wa eleng h o 355 nm and an emission
wa eleng h o 460 nm was used o measu e glyca ed BSA o ma ion. Aminoguanidine (AG, 1 mg) was used as a posi i e
con ol o he s udy.
AGE inhibi ion (%) = [1 − 𝐹𝑠−𝐹𝑠𝑏
𝐹𝑐−𝐹𝑐𝑏] 𝑥 100
Whe e Fs – Fsb is he di e ence be ween he luo escen in ensi y o sample + BSA incuba ed wi h o wi hou glucose
while Fc - Fcb is he di e ence be ween he luo escen in ensi y o BSA incuba ed wi h o wi hou glucose.
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2.4.5. De e mina ion o p o ein ca bonyl con en
Ca bonyl con en is ega ded a glyca ion indica o and is u ilized as a measu e o e alua e p o ein oxida ion as well as
a con i ma o y assay o AGE p oduc ion. The le el o ca bonyl g oup in glyca ed BSA was sligh ly modi ied acco ding
o Le ine’s me hod [22]. Concisely, 100 μl o glyca ed BSA was mixed wi h 400 μl o 10 mM 2,4-dini ophenylhyd azine
(DNPH) in 2.5 M HCl. A e incuba ion o 60 min a oom empe a u e, glyca ed BSA was hen p ecipi a ed using 500
μl o 20 % (w/ ) ichlo oace ic acid (TCA), le on ice o 5 min, and cen i uged a 10,000 g o 10 min a 4 °C. The
p o ein pelle was washed 3 imes by 500 μl o 1:1 ( / ) e hanol: e hyl ace a e solu ion. The inal p o ein pelle was
esuspended in 250 μL o 6 M guanidine hyd ochlo ide. The abso bance was ead a 370 nm. The p o ein ca bonyl g oup
o each sample was calcula ed by using abso p ion coe icien (ɛ=22,000 M−1.cm−1). The p o ein ca bonyl con en was
exp essed as nmol ca bonyl/mg p o ein.
2.5. S a is ical analysis
Da a we e exp essed as means ± s anda d e o o mean (S.E.M), N=3. Da a we e analyzed using One way ANOVA
ollowed by Tukey’s HSD pos hoc es . P- alue
3. Resul s
3.1. To al phenolic con en , e ic educing an ioxidan powe and lipid pe oxida ion
The in e media y pola sol en (e hyl ace a e) pa i ioned majo i y o he phenolic compounds making i he phenol
ich ac ion (Table 1). Lowes con en was ound in he non-pola sol en ac ion (n-hexane) while wa e ac ion
con ained abou double old lowe he quan i y eco ded in e hyl ace a e ac ion.
The ac ions showed g aded concen a ion dependen educ ion o e ic ion o e ous ion (Figu e 1). Using eg ession
equa ion gene a ed om he e ous calib a ion cu e (Y = 0.0009x – 0.1324), he ac ions showed simila end o
e ec based on hei phenolic con en . E hyl ace a e ac ion showed he s onges e ic educing powe while n-hexane
ac ion he leas . These educing powe s shown by he ac ions we e howe e lowe when compa ed o co esponding
concen a ions o he e e ence s anda d (asco bic acid).
Fo he inhibi ion o lipid pe oxida ion, n-hexane ac ion p oduced linea concen a ion-e ec cu e compa ed o o he
ac ions ha p oduced hype bolic cu e shape jus like he e e ence s anda d ( olox) (Figu e 2). The o de o
inhibi ion o lipid pe oxida ion by he ac ions ollowed he same end wi h phenolic con en . E hyl ace a e ac ion
inhibi ed 50% o lipid pe oxida ion a 0.349 mg/ml which is he closes compa ed o olox - he e e ence s anda d
(0.15 mg/ml). n-hexane equi ed up o 6768 mg/ml concen a ion o p oduce same inhibi ion o 50% lipid pe oxida ion.
Table 1 To al phenolic con en o he ac ions o N. lae is ex ac
F ac ions o N. lae is Ex ac
To al Phenolic con en (mgGAE/g)
N-hexane
46.87 + 1.10
E hyl ace a e
389.91 + 4.74
Bu anol
236.85 + 2.56
Wa e
107.79 + 4.02
Whe e GAE = Gallic acid equi alen
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Figu e 1 Fe ic educing an ioxidan powe e ec o he ac ion
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Figu e 2 Inhibi o y e ec o he ac ion on lipid pe oxida ion
3.2. E ec o ea men on ad anced glyca ion end (AGE) p oduc o ma ion
The o ma ion o AGE in bo ine se um albumin (BSA) was measu ed by he luo escence in ensi y. As shown in igu e
3, he luo escen in ensi y inc eased wi h ime du ing 4 weeks o expe imen in he ehicle con ol g oup (BSA-F).
The bu anol and wa e ac ions showed concen a ion dependen inhibi ion o AGE o ma ion. The luo escen
in ensi y eco ded by he g aded concen a ions o he ac ions we e signi ican ly (P<0.05) lowe han ha o he
ehicle con ol a all poin s o measu emen ( igu e 3). The e ec eco ded by hese ac ions we e signi ican ly (P<0.05)
lowe han ha shown by he e e ence s anda d (Aminoguanidine).
The n-hexane ac ion showed lowe abili y o inhibi AGE o ma ion compa ed o o he ac ions. Signi ican (P<0.05)
inhibi ion o AGE o ma ion whe e shown in week 1 a he ini ia ion o AGE o ma ion ( igu e 4). Wi h ime, highe
concen a ions o n-hexane ac ion we e equi ed o p oduce signi ican (P<0.05) inhibi ion o AGE o ma ion. E hyl
ace a e ac ion eco ded he highes e ec o inhibi ion o AGE o ma ion compa ed o o he ac ions as shown by
signi ican ly (P<0.05) lowe luo escen in ensi y compa ed o he ehicle con ol. A week 1, all he es ed
concen a ions excep 0.1 mg/kg showed simila s eng h o inhibi ion o AGE o ma ion compa ed o he e e ence
s anda d wi h no signi ican (P>0.05) di e ence when hese concen a ions we e compa ed be ween g oups. In weeks
2 - 4, 0.4 – 1.6 mg/ml concen a ions o e hyl ace a e ac ion p oduced simila e ec when compa ed o e e ence
s anda d.
The inhibi ion o AGE p oduced by he ac ions ollowed he same end in all he weeks o he expe imen wi h e hyl
ace a e ac ion ha ing he highes inhibi ion while n-hexane he leas ( igu e 5). The hal -maximal inhibi o y
concen a ion o e hyl ace a e ac ion a he end o he expe imen (week 4) was 0.058 mg/ml while ha o n-hexane
was 1575 mg/ml. Simila ly, bu anol and wa e ac ions equi ed highe concen a ions o inhibi 50% o AGE o ma ion
compa ed o e hyl ace a e ac ion ( igu e 6). Howe e , hese pola ac ions (bu anol and wa e ac ions) p oduced
be e han he pola ac ion (n-hexane ac ion).
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Whe e: * = P<0.05 compa ed o BSA-F ( ehicle con ol); # = P<0.05 compa ed o Aminoguanidine (s anda d e e ence d ug). Whe e BF = bu anol
ac ion and WF = wa e ac ion
Figu e 3 E ec o bu anol and wa e ac ions on Ad anced glyca ion end p oduc o ma ion
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Figu e 4 E ec o Hexane and E hyl ace a e ac ions on Ad anced glyca ion end p oduc o ma ion
Whe e: * = P<0.05 compa ed o BSA-F ( ehicle con ol); # = P<0.05 compa ed o Aminoguanidine (s anda d e e ence d ug). Whe e HF = hexane
ac ion and EF = E hyl ace a e ac ion
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Figu e 5 G aded concen a ion e ec o sol en ac ions o N. lae is ex ac on inhibi ion o Ad anced glyca ion end
p oduc o ma ion
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