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REVIEW a icle
An i-aging po en ials o a polyphenol- ich supplemen om A ican
So ghum bicolo lea shea hs: A na a i e e iew
Paul A. Adeleke 1 , Olajuwon Okubena 1, 2 , Abimbola Okubena 1, 2 , Abayomi M. Ajayi 1
Ololade Okubena 1, 2 , Fa ou B. Jegede 1 , and Solomon Umuko o 1 *
1 Depa men o Pha macology and The apeu ics, College o Medicine, Uni e si y o Ibadan, Ibadan, Oyo S a e, Nige ia
2 Depa men o Pha macology and The apeu ics, College o Medicine and Heal h Sciences, A e Babalola Uni e si y, Eki i, Nige ia
A icle numbe : 231, Recei ed: 02-11-2025, Accep ed: 25-11-2025, Published online: 00-11-2025
HOW TO CITE THIS
Adeleke e al. An i-aging po en ials o a polyphenol- ich supplemen om A ican So ghum bicolo lea shea hs: A na a i e e iew.
Medi e J Pha m Pha m Sci. 2025; 5(4): 58-77. [A icle numbe : 231]. h ps://doi.o g/10.5281/zenodo.17742769
Keywo ds: Age- ela ed disease, an i-in lamma o y, an ioxidan , neu op o ec ion, So ghum bicolo supplemen
Abs ac : Aging is a complex biological p ocess ma ked by a g adual decline in physiological unc ions and
sys emic de e io a ion, esul ing in inc eased suscep ibili y o age- ela ed diseases. The e is inc easing in e es in
he use o plan -based cons i uen s in mi iga ing oxida i e s ess and in lamma ion, he majo d i e s o aging and
age- ela ed diseases. Polyphenol- ich plan -based cons i uen s including So ghum bicolo supplemen (SBS) wi h
po en an ioxidan , an i-in lamma o y and neu op o ec i e p ope ies, ha e demons a ed an i-aging po en ial. The
aim o his e iew is o p o ide documen a ion om published li e a u e on he an i-aging po en ials o SBS ha
may elici he need o i s clinical e alua ion o age- ela ed diseases. A li e a u e sea ch was conduc ed using
PubMed elec onic da abase wi h subjec headings, ela ed o he mechanisms o aging, age- ela ed diseases,
heal h bu den o aging popula ion, and polyphenols o a heal hy li e span. I also included he sou ce, bioac i e
cons i uen s, and an iaging po en ial o SBS. The indings ob ained om he e iew showed ha SBS mi iga ed
age- ela ed diseases in a ious animal models. The supplemen ex ended he li e span o D osophila melanogas e
and imp o ed hei mo o unc ions. The SBS inhibi ed he ac i i y o collagenase and elas ase enzymes in ol ed
in p ema u e skin aging and exhibi ed cy op o ec ion agains hyposaline-induced ed blood cells hemolysis. The
an i-aging po en ial o SBS ela es o i s po en an ioxidan , an i-in lamma o y, immune-modula ing, and neu o-
p o ec i e p ope ies. These indings p o ide a s ong ounda ion o u he p eclinical and clinical s udies o
alida e he he apeu ic po en ials o SBS in p omo ing a heal hie li espan and enhancing he quali y o li e o
he aging popula ion.
In oduc ion
Aging is a complex, i e e sible, and ine i able biological p ocess ma ked by a g adual decline o physiological
unc ions and sys emic de e io a ion, esul ing in inc eased suscep ibili y o age- ela ed diseases [1]. Oxida i e
s ess and in lamma ion a e key d i e s o aging, con ibu ing o elome e a i ion, DNA damage, mi ochond ial
dys unc ion, gene ic ins abili y, immune impai men , and me abolic diso de s [2, 3]. Aging inc eases he
incidence and se e i y o he debili a ing na u e o age- ela ed diseases such as ce eb o ascula diso de s,
neu odegene a i e diseases, diabe es, isual impai men , musculoskele al diso de s, and cance [4, 5]. Thus, when
Copy igh © 2025. This open-access a icle is dis ibu ed unde he C ea i e Commons A ibu ion License, which pe mi s
un es ic ed use, dis ibu ion, and ep oduc ion in any medium, p o ided he o iginal wo k is p ope ly ci ed.
Medi e anean Jou nal o
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aging eaches a ce ain c i ical h eshold, o gan and issue unc ions apidly de e io a e, inc easing he incidence
and mo ali y o age- ela ed diseases. Howe e , he dec ease in physical s eng h and cogni i e impai men s,
pa icula ly demen ia, a e he p ominen ea u es o he aging p ocess. In e es ingly, aging and ch onic diseases
a e highly associa ed wi h inc eased oxida i e s ess, ele a ed ch onic low-g ade in lamma ion and inc eased
DNA damage [6, 7]. Al hough he p ospec o inc eased li espan is desi able, he e is a need o conside he
challenges o disabili y and he bu den o li ing wi h age- ela ed diseases. No ably, he quali ies o li e o mos
elde ly people a e g ossly impai ed ins ead o a heal hy li e span [8].
Globally, he p opo ion o olde people (aged 60 yea s and abo e) is ising, and i has been es ima ed ha i will
nea ly double by 2050 [9]. De eloping na ions a e unde going apid demog aphic ansi ions, wi h he ise o
aging popula ions [10]. The inc ease in he global aging popula ion, age- ela ed diseases he ocus o a en ion
wo ldwide o se e al easons. Fo example, he unc ional decline in he elde ly poses se ious challenges, a ising
om he inc eased bu den o age- ela ed diseases and he sho ening o heal hy li e span. Aging comes wi h
inancial p essu e in e ms o loss o economic p oduc i i y and medical expenses [1, 11]. The e o e, i is highly
impe a i e o sea ch o e ec i e in e en ions ha can posi i ely p olong he heal hy li espan o he aging
popula ion. The cu en ocus o aging esea ch has shi ed owa ds in e en ions a ge ing oxida i e s ess and
in lamma ion o p omo e no jus longe i y bu a heal hie li espan [1, 11]. Phy ochemicals ha e shown p omising
e icacies in add essing he mul i ace ed pa hways associa ed wi h aging [1, 12, 13]. The polyphenol- ich SBS
de i ed om he lea shea hs o he A ican So ghum bicolo a ie y has demons a ed an ioxidan , an i-
in lamma o y, immune modula ing, and neu op o ec i e p ope ies in a ious expe imen al models [14-16]. In
addi ion, hese bioac i e cons i uen s can mi iga e aging- ela ed diseases and p omo e heal hy li ing among he
elde ly. Ne e heless, a ailable expe imen al da a on SBS ha e ye o be ex ensi ely e iewed o highligh i s
an i-aging po en ial o a heal hy long li e-span. Consequen ly, his e iew unde sco es i s an i-aging p ope ies,
based on in o ma ion om he PubMed elec onic da abase. The indings ob ained om he e iew can p o ide a
s ong ounda ion o u he p eclinical and clinical s udies o alida e he he apeu ic po en ial o SBS in
p omo ing a heal hie li espan and quali y o li e o he aging popula ion.
Li e a u e sea ch s a egy: This e iew analyzed in o ma ion ob ained om a comp ehensi e sea ch o li e a u e
using he PubMed elec onic da abase wi h he subjec headings, ela ing o mechanisms o aging, age- ela ed
diseases, heal h bu den o aging popula ion, and polyphenols o a heal hy li e span. The sea ch includes he
sou ce, bioac i e cons i uen s, and an iaging po en ial o SBS. We excluded s udies wi h non-a ailabili y o he
ull- ex a icles, pe sonal opinions and hose no w i en in he English language.
Discussion o key indings: The published a icles e ie ed based on he li e a u e sea ch, we e discussed, mainly
on ou b oad ca ego ies, including heal h ca e bu den o he elde ly, biological basis o aging, polyphenols o
aging and an iaging p ope ies o SBS. The an iaging p ope ies o SBS we e u he discussed unde ou b oad
sub opics.
Heal h ca e bu den o he elde ly: Globally, he p opo ion o olde people, 60 yea s and abo e, is on he inc ease
and i has been es ima ed ha i will double by 2050 [9]. Howe e , he aging popula ion has se e al consequences
on economies, social se ices and heal hca e sys ems, and hey a e o en associa ed wi h di e ing le els o
disabili y and a de e io a ing quali y o li e. The unc ional decline in he elde ly poses se ious challenges as well
as inancial p essu es in e ms o educed p oduc i i y and cos o medical expenses [5, 17]. Financial and
economic ac o s signi ican ly a ec heal h ou comes and well-being o elde ly people. Speci ically, s udies ha e
shown ha disease bu dens can lead o a dec ease in economic g ow h and inc eased amilies’ heal h- ela ed
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expendi u e [5, 18, 19]. In ac , he bu den o diseases among he elde ly people could inc ease amilies’
ca egi ing liabili y, a ec ing esou ce alloca ion and labo employmen wi hin he household [18, 19]. The need
o ca egi ing can a ec household income and esou ces, pa icula ly o amilies ca ing o elde ly ela i es
wi h disabili ies.
The impac s o he aging popula ion on heal h sys ems ha e been documen ed in he li e a u e. Fo example, i
has been epo ed ha in he Uni ed S a es, people aged 65 and abo e, accoun ed o 30% o heal hca e
expendi u e in 2008, a igu e expec ed o ise o 50% by he yea 2030 [5, 20]. In Sub-Saha an A ica, he e ec s
o aging would e en be mo e de as a ing in coun ies like Nige ia, Ghana, Kenya, and Uganda, because o he
p ojec ed inc ease in he numbe o olde adul s [21]. Taken oge he , hese obse a ions sugges he need o
de elop he apeu ic s a egies ha can enhance he quali y o li e o he aging popula ion.
Biological basis o aging: The ema kable in luence o aging on he genesis o ch onic diseases in humans and
hei p og ession highligh s he need o unde s and he basic mechanisms ha unde lie he aging p ocess and
human longe i y. Unde s anding he key molecula and cellula p ocesses ha a e in ol ed in aging may p omo e
he de elopmen o he apeu ic agen s ha could delay senescence and imp o e o e all human heal h [22].
Al hough he dilemma behind why we age, and he causes o aging appea un a homable, a ple ho a o heo ies
ha e been p opounded o e he yea s o un a el he complex na u e o he aging p ocess [23]. These include
elome e a i ion, DNA damage, mi ochond ial dys unc ion, loss o nico inamide adenine dinucleo ide (NAD+)
le els, impai ed au ophagy, s em cell exhaus ion, in lamma ion, loss o p o ein balance, oxida i e s ess,
de egula ed nu ien -sensing, al e ed in e cellula communica ion and dysbiosis [1, 22, 24]. The de egula ion o
hese in e connec ed pa hways leads he cells o a s a e o senescence, which con ibu es o aging and he genesis
o age- ela ed diseases (Figu e 1). Indeed, many o hese in e ela ed mechanisms, especially DNA damage, ha e
been ou ed as d i e s o aging [24].
Figu e 1: Key documen ed molecula basis o aging and age- ela ed diseases
Telome e a i ion, DNA damage, mi ochond ial dys unc ion, loss o nico inamide adenine dinucleo ide le els, impai ed mac o-
au ophagy, s em cell exhaus ion, in lamma ion, loss o p o ein balance, de egula ed nu ien sensing, al e ed in e cellula
communica ion, and dysbiosis a e some o he key p ocesses ha unde lie aging [1]. Aging leads o o gan/sys emic de e io a ion and
an inc ease in suscep ibili y o age- ela ed diseases such as ca dio ascula , ce eb o ascula , degene a i e join disease, diabe es,
Pa kinson’s disease, Alzheime ’s disease and cance [1].
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DNA damage is he majo in e nal ac o ha igge s genomic ins abili y, epigene ic changes, p o ein s ess,
impai ed mi ochond ial unc ion, and elome e dys unc ion [1, 25]. No ably, he con inuous accumula ion o
DNA-damaged cells igge s cell dea h and senescence, e en ually leading o ch onic in lamma ion, loss o
unc ion, a ophy, and aging o cells and issues [26]. Ne e heless, he unanswe ed ques ion abou wha ac o
igge s DNA damage, ab ini io, sugges s ha iden i ying, which o he in e - ela ed mechanisms a e d i e s o
passenge s o aging emains a big challenge [24]. Howe e , he ee adical o oxida i e heo y appea s o be he
mos popula heo y o aging, wi h se e al s udies demons a ing he inju ious na u e o excessi e eac i e oxygen
species (ROS) and oxida i e s ess ia mechanisms, ela ing o he sho ening o elome es, mi ochond ial
dys unc ion, and he ini ia ion o aging- ela ed in lamma o y esponses [27]. The heo y also has a lo o e idence-
based suppo [28]. P oposed by Ha man in 1956, he ee adical heo y holds ha aging is associa ed wi h he
accumula ion o ROS ha exe oxida i e damage o cellula biomolecules, especially he DNA (Figu e 2),
ul ima ely leading o a decline in physiological unc ion and dea h [29]. The cellula degene a ion and ea ly
apop osis caused by ee adicals p oduce oxida i e s ess, ega ded as he main pa hological culp i in p ema u e
aging [29]. Mo eo e , oxida i e s ess is u he agg a a ed by a a ie y o s esso s, which may accele a e aging
and age- ela ed diseases, as well as inc eased ulne abili y o dea h [30].
Figu e 2: Role o ee adicals in oxida i e s ess and he aging p ocess [3]
The ee adical heo y holds ha aging is associa ed wi h he accumula ion o ROS ha exe oxida i e damage o cellula
biomolecules, especially he DNA, ul ima ely leading o a decline in physiological unc ion and causing cellula dea h [29].
The cellula degene a ion and ea ly apop osis caused by ee adicals p oduce oxida i e s ess, which is ega ded as he main
pa hological culp i in p ema u e aging [27, 29]
Indeed, oxida i e s ess and in lamma ion unde lie he elome e a i ion, DNA damage, mi ochond ial
dys unc ion, gene ic ins abili y, impai ed immune unc ions and me abolic de egula ions (Figu es 3-5) ha
unde pin he aging p ocess [1]. The accumula ion o ROS ha exe s oxida i e damage o cellula biomolecules
and apop osis migh be he p ima y ini ia o o he complex in e connec ed pa hways ha lead o de e io a ion in
bodily unc ion wi h aging. As shown in Figu es 4 and 5, ROS induces elome e damage, leading o i s sho ening
and decapi a ion, which u he suppo s he cen al ole o oxida i e s ess in he aging p ocess. ROS and
de egula ed me aboli es (NAD+) con ibu e o mi ochond ial dys unc ion, and he de elopmen o se e al age-
ela ed diseases [1]. S udies ha e shown ha inc eased ROS le els con ibu e o dec eased eplica ion o s em
cells [31]. In addi ion, senescen cells sec e e p o-in lamma o y cy okines, and s udies ha e shown ha ROS and
in lamma ion a e all impo an induce s o cell senescence [32].
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Figu e 3: D i e s o DNA damage and he esul ing sys emic consequences o loss o cellula unc ions
and he genesis o age- ela ed diseases [1]
The sou ces o a ious inju ious subs ances ha cause gene ic abno mali ies, dys unc ional elome es, epigene ic al e a ions, and
mi ochond ial dys unc ion ha e been es ablished in he li e a u e [1, 3]. Ul ima ely, DNA damage leads o cellula dys egula ions
and p omo es he de elopmen o age- ela ed diseases [1]
Figu e 4: The ole o ROS in elome e decapi a ion and accele a ed cell senescence [1]
ROS ha e been implica ed in elome e decapi a ion and accele a ed cell senescence [1]. Accumula ed senescen cells a e known o
sec e e a complex se o p o-in lamma o y cy okines, he senescence-associa ed sec e o y pheno ype (SASP), which enhances T cells
and mac ophages, esul ing in sys emic ch onic in lamma ion and in lamma ion- ela ed diseases [1].
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Figu e 5: D i e s o mi ochond ial dys unc ion and de elopmen o se e al age- ela ed diseases [1]
Heal hy mi ochond ial me abolic unc ion is a key ac o in ensu ing long- e m heal h du ing he aging p ocess and
is suscep ible o a ious en i onmen al ac o s and endogenous me aboli es. Al e a ions in mi ochond ial unc ion ha e
widesp ead ad e se e ec s on in acellula homeos asis and lead o sys emic o gan decline and he de elopmen
o se e al age- ela ed diseases h ough complex signaling mechanisms [1]
In e ms o aging, exposu e o sou ces o damage o e he human li espan a ies among indi iduals and may
pa ly explain why people age di e en ly [33]. Howe e , he ee adical heo y has ecen ly aced se e e
c i icisms [34] including ailu e in add essing some c i ical aspec s o aging. This ealiza ion has led some au ho s
o sugges ha he ee adical heo y o aging needs o be modi ied and imp o ed upon. I likewise echoes he
no ion ha no single heo y has been able o explain he mechanism o aging [34] and none is gene ally conside ed
as he gold s anda d [35]. Al hough he ex an heo ies on aging o en compe e and con lic wi h one ano he , a
maximally co ec heo y may igge signi ican b eak h oughs in he disco e y o an iaging in e en ions. This
may come ia he in eg a ion o some exis ing heo ies o a be e unde s anding o he mechanisms o aging and
de elopmen o an iaging he apy [34]. Ne e heless, he ee adical heo y o aging is s ill one o he mos
p omising heo ies o aging and cons i u es he p ima y a ge o an iaging esea ch. An imbalance be ween ee
adical gene a ion and an ioxida i e capaci y causes oxida i e damage o DNA, p o eins, and mi ochond ia du ing
he aging p ocess. In e es ingly, Auley e al. [36] had u he highligh ed he signi ican ole o oxida i e s ess in
he ne wo k heo y o aging, as in e ac ions be ween he di e en key mechanisms ela ing o de ec i e
mi ochond ia, oxida i e s ess, DNA damage, and dys egula ion o cellula signaling (Figu e 6). Addi ionally,
an ioxidan supplemen a ion has been shown o e a d he aging p ocess and delay he onse o age- ela ed
diseases, as well as ex end human heal h and longe i y [3]. Owing o hese packe s o scien i ic knowledge,
cu en an iaging esea ch is p ima ily ocused on he use o an ioxidan polyphenolic compounds o p omo e no
only longe i y, bu a heal hie li espan [3].
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Figu e 6: Complex pa e ns o in e ac ions be ween oxida i e s ess, DNA, p o ein damage,
mi ochond ial dys unc ion and dys egula ion o cellula signaling in aging p ocess [36]
The dys egula ion o hese in e connec ed pa hways makes he cells senescen , con ibu ing o aging and he genesis
o age- ela ed diseases [24]. The accumula ion o ROS ha exe s oxida i e damage o cellula biomolecules and apop osis
migh be he p ima y ini ia o o he complex in e connec ed pa hways ha lead o de e io a ion in bodily unc ion du ing aging.
Polyphenolic plan -based p epa a ions o aging
The desi e o slow down he aging p ocess and ex end heal hy li e span has been he igo ous pu sui o he
scien i ic ield in ecen imes. The ad ocacy o li es yle changes, including calo ie es ic ion, sleep egula ion,
and exe cise, has been epo ed o be insu icien in ex ending he heal hy li espan o olde people o p e en ing
age- ela ed diseases [1]. Thus, many s udies ha e ocused on he mechanisms unde lying he aging p ocess and
explo ing ways o a ge ing he hallma k ea u es o aging, pa icula ly oxida i e s ess and in lamma ion.
Polyphenolic- ich phy ochemicals ha e shown p omising an iaging p ope ies by a ge ing he mul i ace ed
pa hways associa ed wi h aging. They exhibi nume ous biological ac i i ies; including an ioxidan e ec s, ee
adical sca enging, an i-in lamma o y p ope ies, neu op o ec ion, and immunomodula ion pha macological
a ge s o an iaging s udies [37, 38].
Polyphenolic compounds, ound abundan ly in plan -based oods, a e inc easingly being ecognized o hei
po en ial an i-aging p ope ies. Polyphenols a e essen ial componen s o human die s, and epidemiological da a
indica e ha consuming oods ich in an ioxidan s lowe s he incidence o oxida i e s ess- ela ed aging diso de s
such as diabe es, ca dio ascula diseases, neu odegene a i e diseases and cance [12, 13]. These compounds can
help comba cellula damage, imp o e a ious physiological unc ions, and po en ially slow down he aging
p ocess. Indeed, polyphenols p o ec cells om oxida i e s ess, delay cellula aging, and sa egua d issues om
deg ada ion [38]. Ce ain polyphenols can educe in lamma ion, a key d i e o age- ela ed condi ions, by
supp essing in lamma o y signaling pa hways. In addi ion, polyphenolic compounds a e gene ally ega ded as
sa e and e ec i e in p e en ing age- ela ed diseases [38, 39].
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Die a y polyphenolic componen s can ex end he li espan o a ious model species by emo ing senescen cells,
main aining mi ochond ial homeos asis, supp essing in lamma o y esponse, and coun e ing oxida i e s ess [12,
13]. In ac , inc easing e idence has demons a ed ha die a y polyphenol in ake can delay aging and age- ela ed
diseases [38]. The an iaging po en ial o hese phy ocons i uen s is ela ed o hei an i-in lamma o y and
an ioxidan capabili ies and p omo ion o cellula epai [12, 40]. Also, polyphenols can egula e immune unc ion
and imp o e esis ance o diseases by inhibi ing he NF-κB pa hway and p o-in lamma o y gene exp ession,
supp essing he enzymes ela ed o he p oduc ion o ROS, and up- egula ing o he endogenous an ioxidan
enzymes [41]. Polyphenols ha e shown p o ec i e e ec s on cogni i e unc ions, alle ia ing neu odegene a i e
diseases by p e en ing cellula damage, and enhancing DNA epai machine y [42]. Epidemiological s udies
show ha adhe ing o he Medi e anean die a y pa e n, which is a plan -based die , was associa ed wi h be e
heal h ou comes du ing aging [43]. These indings u he sugges ha die s ich in polyphenol-based ood plan s
posi i ely in luence he hallma k o aging- ela ed disease isks and longe i y [43]. Rema kably, die s ich in
ege ables and ui s wi h an ioxidan and an i-in lamma o y ac i i ies a e linked o a low incidence o age- ela ed
diseases [44, 45]. Based on hese indings, i is logical o hink ha he nu ien s and bioac i e molecules ound
in plan -based oods play a key ole in ac ing syne gis ically o posi i ely in luence he di e en pa hways o he
aging p ocesses.
An iaging p ope ies o he SBS supplemen
So ghum bicolo (L. Moench, amily Poaceae), popula ly known as mille , swee So ghum, o guinea co n, is
widely cul i a ed in many opical coun ies o he wo ld o i s economic, nu i ional, and medicinal alues [14].
So ghum bicolo is a unique plan -de i ed ood and anked i h a e whea , maize, ice, and ba ley in he wo ld’s
ce eal p oduc ion [46]. Besides being used as a s aple ood by he na i es o A ica, Cen al Ame ica and Sou h
Asia, he so ghum g ain is used wo ldwide as animal eed [47]. In e hnomedicine, di e en pa s o he plan ,
including he g ain, a e used o a my iad o ch onic diseases [14, 47]. Howe e , he lea -shea hs po ion o he
plan ha e been ecognized o he p esence o high con en s o polyphenolic bioac i e compounds (Table 1).
These bioac i e compounds ha e exhibi ed po en an ioxidan , an i-in lamma o y, immunomodula ing and
neu op o ec i e, and chemop e en i e p ope ies [14, 16, 48], sugges ing he po en ial oles o SBS in mi iga ing
age- ela ed diseases and as a possible elixi o heal hy aging. In his e iew, we p esen e idence om he
li e a u e alluding o he an iaging po en ial o SBS and i s capaci y o p omo e heal hy aging.
The apeu ic po en ial o SBS supplemen in aging- ela ed diseases
The an iaging po en ial o SBS is implied in i s epo ed mi iga ion o age- ela ed diseases such as s oke, a h i is,
cance , mo emen diso de s, and memo y de ici s [14]. I is wo h no ing ha ischemic s oke is he second
leading global cause o dea h and physical disabili ies among he elde ly. I is due o he ac i a ion o oxida i e
and in lamma o y pa hways igge ed by he obs uc ion o ce eb al blood low and subsequen neu onal cell
dea h [49]. Thus, a ge ing oxida i e and in lamma o y pa hways wi h bioac i e cons i uen s o plan o igins
o e s p omising he apeu ic s a egies o ischemic s oke [49-51]. Epidemiological da a ha e e ealed ha
egula consump ion o plan -based oods ich in polyphenols can educe he isk o s oke [51]. Lending c edence
o his, p eclinical s udies showed ha SBS educes he neu ological de ici s in a global ischemic s oke model
h ough inhibi ion o oxida i e s ess, p o-in lamma o y cy okines (IL-6 and TNF-α) and NF-kB eac i i y in a s
[52]. I p o ec ed he neu ons o he s ia um, p e on al co ex, and hippocampus, as well as inc easing he
popula ion o iable neu onal cells in hese b ain egions o ischemic a s [52]. The po en ial bene i s o SBS in
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neu odegene a i e diseases like Alzheime ’s disease (AD) and Pa kinson’s disease (PD) ha e also been
in es iga ed in scopolamine-induced amnesia and o enone-induced mo o dys unc ions, espec i ely, [53, 54].
The indings showed ha he supplemen a enua ed amnesia and mo o dys unc ions by augmen ing he neu onal
an ioxidan p o ec i e mechanisms. I educed p o-in lamma o y cy okines in o enone-induced Pa kinsonian-like
mo o dys unc ions in a s [54], indica ing i s he apeu ic po en ial in mo emen - ela ed diso de s associa ed wi h
aging.
Rheuma oid a h i is is ano he age- ela ed disease in he elde ly. I is a ch onic in lamma o y au oimmune disease
due o p og essi e in lamma ion o he syno ial issues, and ca ilage des uc ion in he a ec ed join s [55, 56].
The join s’ heal h-p omo ing e ec s o SBS was demons a ed when i was es ed in a s subjec ed o in a-
a icula injec ion o comple e F eund's adju an (CFA). The supplemen was shown o ha e educed pain
sensi i i y in he hype algesia es and join in lamma ion in a s wi h in a-a icula injec ion o CFA. The
supplemen also posi i ely modula ed oxida i e s ess, p o-in lamma o y cy okines, apop o ic ac o s (caspase 3
and caspase 9), NF-κB, myelope oxidase, and nuclea ac o e y h oid 2- ela ed ac o 2 (N 2), and a icula
issue degene a ion in he ankles o CFA-a h i ic a s [57]. No ably, hese bioma ke s and ansc ip ion ac o s
(NF-κB and N 2) play pi o al oles in cellula aging and age- ela ed pa hologies, including a h i is [58-59].
Thus, he indings ha SBS posi i ely modula ed hese biochemical pa hways and ansc ip ion ac o s u he
subs an ia e i s an i-aging po en ial in p omo ing heal hy join s in he elde ly. S udies ha e shown ha SBS is ich
in di e se bioac i e polyphenol- ich cons i uen s (Table 1) such as lu eolin, na igenin, apigenindin, apigenin and
lu eolinidin [16, 60], mos o which exe di e se pha macological ac i i ies; including an i-in lamma o y, an i-
mu agenic, an icance , immunomodula o y, an ioxidan , and neu op o ec i e e ec s [16, 61, 62]. SBS is ich in
mine als such as i on, zinc, calcium, coppe , magnesium, selenium, phospho us, sodium and po assium, and
omega-6 a y acid [14], which a e essen ial o me abolism and neu onal unc ioning [63]. Omega-3 and -6 a y
acids, o example, ha e demons able an i-in lamma ion, an i-apop osis and neu op o ec i e p ope ies [64, 65].
Table 1: Phy ochemical cons i uen s o lea shea hs o So ghum bicolo , Jobelyn® [60]
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Au ho s’ con ibu ion: AAA, SU, AMA, OO & MOSA. concei ed and designed he s udy. SU, MOSA, LOO & FBJ. w o e he
d a and edi ing. All au ho s e iewed and app o ed he inal e sion o he manusc ip .
Con lic o in e es : The au ho s decla e he absence o any comme cial o inancial ela ionships ha could be cons ued as a
po en ial con lic o in e es .
E hical issues: The au ho s comple ely obse ed e hical issues, including plagia ism, in o med consen , da a ab ica ion o
alsi ica ion, and double publica ion o submission.
Da a a ailabili y s a emen : The aw da a ha suppo he indings o his a icle a e a ailable om he co esponding au ho upon
easonable eques .
Au ho decla a ions: The au ho s con i m ha hey ha e ollowed all ele an e hical guidelines and ob ained any necessa y IRB
and/o e hics commi ee app o als.
Gene a i e AI disclosu e: No Gene a i e AI was used in he p epa a ion o his manusc ip .
