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Role ofHerbal Medicines
https://t.me/medicina_free
fortheTreatment ofChronic Kidney
Disease
VafaBaradaran Rahimi andVahidRezaAskari
Abstract
The use of herbal medicines has tremendously increased
globally and in developed countries over the past decades.
Nowadays, several herbal medicines are used to treat many
chronic and acute disorders, including chronic kidney diseases (CKD). The promising effects of many of them are
well investigated and documented by researchers worldwide. This chapter focuses on the promising anti-CKD
effects of Abelmoschus manihot, Salvia miltiorrhiza, and
their constituents, salvianolic acid-A, salvianolic acid-B,
and tanshinone-IIA, berberine, Zingiber ofcinale, and its
constituents 6-gingerols and 6-shogaols, Punica granatum
and its major constituent ellagic acid, Vitis vinifera,
Curcuma longa, and their major constituent curcumin,
Nigella sativa, Rosmarinus ofcinalis, and their major
constituent rosmarinic acid, in different animal and human
clinical studies. CKD was mainly treated with these herbal
medicines through anti-oxidative, anti- inammatory, anti-
brotic, and anti-apoptotic effects, improving renal function, downregulating the nuclear factor-kappa B (NF-κB)
signaling pathway, and stimulating the nuclear factor erythroid 2-related factor-2 (Nrf-2) cascade.
Keywords
Chronic kidney disease · NF-κB · Inammation · Herbal
medicines · Oxidative stress
1 Introduction
Herbal medicines with promising anti-chronic kidney disease (CKD) effects are illustrated in Fig.1. Table1 summarizes herbal medicine’s protective effects against animal
models of CKD.In addition, human clinical studies supporting the anti-CKD effects of herbal medicines are shown in
Table2.
V. BaradaranRahimi
Department of Cardiovascular Diseases, Faculty of Medicine,
Mashhad University of Medical Sciences, Mashhad, Iran
e-mail: baradaranrv@mums.ac.ir
V. R. Askari (*)
Applied Biomedical Research Center, Mashhad University of
Medical Sciences, Mashhad, Iran
International UNESCO Center for Health-Related Basic Sciences
and Human Nutrition, Mashhad University of Medical Sciences,
Mashhad, Iran
e-mail: askariv@mums.ac.ir
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023
A. K. Dhara, S. C. Mandal (eds.), Role of Herbal Medicines, https://doi.org/10.1007/978-981-99-7703-1_15
293
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V. BaradaranRahimi and V. R. Askari
Fig. 1 Herbal medicines with promising anti-CKD effects
Table 1 Protective effects of herbal medicines against animal models of CKD
Extract or constituent type Dose/concentration An overview of the study model Results References
Abelmoschus manihot
(HKC)
Abelmoschus manihot
(HKC)
Abelmoschus manihot
(HKC)
Abelmoschus manihot
(HKC)
75, 175, and 300mg/
kg/day; given orally for
12weeks
0.75 and 2.0g/kg/day;
orally for 8 weeks
0.5 and 2.0g/kg/day;
orally for 4 weeks
2.0g/kg/day; orally for
4 weeks
Unilateral nephrectomy and
streptozotocin-induced DN in
male Sprague-Dawley rats
Unilateral nephrectomy and
streptozotocin- induced DN in
male Sprague-Dawley rats
Unilateral nephrectomy and
adriamycin-induced nephropathy
in male Sprague-Dawley rats
Unilateral nephrectomy and
adriamycin-induced nephropathy
in male Sprague-Dawley rats
↓ TGF-β and collagen type IV
expression in the kidney
↑ PPAR-α, CPT-1, and ACO
expression
↑ PPAR-γ, CD36, and LPL
expression
↑ Serum adiponectin
↓ TNF-α, IL-6, IL-1β and IL-2
↓ BUN and UA levels
↓ Urinary albumin levels
↓ Oxidative stress parameters,
including MDA, 8OhDG, and NOX4
↑ Anti-oxidant SOD activity
↓ Phosphorylated p38MAPK,
phosphorylated Akt (p-Akt), TNF-α,
and TGF-β protein expressions in the
kidney
↑ Body weight and general status
↓ Kidney/body weight ratio, urinary
protein, serum BUN, and Cr levels
↓ Protein expression levels of TNF-α,
IL-2, TGF-β1, and p-p38MAPK
↓ Body weight, serum albumin, Cr,
and urinary albumin levels
Improved glomerular pathological
changes
↓ p-Akt, p-mTOR, p-p70S6K, and
TGF-β1
[3]
[4]
[5]
[6]
Role ofHerbal Medicines fortheTreatment ofChronic Kidney Disease
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Table 1
(continued)
Extract or constituent type Dose/concentration An overview of the study model Results References
Abelmoschus manihot
(HKC)
70% ethanolic extract of
ower and leaf of
Abelmoschus manihot
Ethyl acetate extract of
Salvia miltiorrhiza
SAA 10mg/kg; orally for 8
SAA 2.5, 5, and 10mg/kg;
SAA 2.5, 5, and 10mg/kg;
SAA 10mg/kg; injected into
SAB 3, 6.25, and 12.5mg/
SAB 50, 100, and 200mg/
SAB 6.25, 12.5, 25mg/kg;
Tanshinone IIA 10mg/kg; oral
0.75g/kg/day; orally
for 4 weeks
100mg/kg/day; orally
for 5 weeks
30mg/kg/day; orally
for 18weeks
weeks
daily, given I.P. over
28days
daily, given I.P. over 28
days
the tail vein for 3 weeks
kg; given I.P. for 4
weeks
kg; administered orally
given for 14days
administration over
12weeks
Induction of chronic renal failure
in rats by adenine
High-fat diet, unilateral
nephrectomy, and streptozotocininduced nephropathy
Streptozotocin-induced DN in
C57BL/6 mice
5/6 nephrectomized rats
5/6 nephrectomized rats
5/6 nephrectomized rats
Adriamycin-induced MCD rat
model
Renal tubular damage by fatty
acid in C57BL/6 mice
Balb/c mice suffering from renal
ischemia-reperfusion injury
Kidney injury by unilateral
ureteral obstruction in C57BL/6
mice
Streptozotocin-induced DN
↓ Serum Cr, BUN, and urinary
protein
↓ NOX1, NOX2, NOX4, α-SMA,
p-ERK expression
↓ Serum Cr, BUN, urinary albumin,
glomerular, and tubular damage
↓ TNF-α, IL-6
↑ IL-10in kidney tissue
↓ Urinary albumin excretion,
albumin/creatinine ratio, serum Cr,
BUN
Improved the pathological changes in
kidney tissue
↑ Nrf-2, HO-1, and NQO1 mRNA
expression
↓ Keap-1in kidney tissue
↓ Kidney/body weight ratio, Scr,
BUN, creatinine clearance rate, and
MDA level
↑ Body weight and SOD activity
↓ TGF-β1in kidney tissue
↑ BMP-7 and Smad6 expression
↓ Urine protein, BUN, Scr
↓ TGF-β1, α-SMA, TNF-α, IL-1β
expression levels
↓ NF-κB and MAPK signaling
cascade
↓ ICAM-1 VCAM-1
↑ SOD and CAT activities
↓ MDA, ROS, and NOX-4 levels
↑ p-Akt, p-Nrf-2, and HO-1in kidney
tissue
↓ Scr, BUN, urinary levels of Angptl4
↑ PPARγ expression in the kidney
tissue
↓ Urinary output, cystatin C, Scr
↓ ICAM-1, VCAM-1, IL-1β and 6,
and TNF-α mRNA expression in
renal tissue
↓ Apoptotic Bax and cleaved
caspase-3 expression
↑ Anti-apoptotic BCL-2 expression
↓ Scr, BUN
↓ MDA, IL-1β, and TNF-α levels
↓ Keap-1
↑ Nrf-2 and HO-1
↑ SOD and GSH activities in kidney
tissue
↓ BUN, Scr
↓ α-SMA, FGF-2, TGF-β1
expression
↑ E-cadherin protein expression in
kidney tissue
↓ Urine albumin excretion rate, CRP,
and MDA levels
↑ SOD activity
↓ TGF-β1, P-selectin, and MCP-1
mRNA expression in kidney tissue
[7]
[8]
[12]
[13]
[14]
[15]
[16]
[17]
[18]
[19]
[20]
(continued)
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(continued)
Table 1
Extract or constituent type Dose/concentration An overview of the study model Results References
Tanshinone IIA I.P. doses of 2, 4, and
Tanshinone IIA 25mg/kg; S.C. Contrast-induced nephropathy
Berberine 200mg/kg; given orally
Berberine Oral dosage of 25 and
Berberine 400mg/kg; orally for
Berberine Eight weeks of oral
Berberine 50, 100, or 200mg/kg;
Berberine 50, 100, or 200mg/kg;
Berberine 100mg/kg; taken for
Berberine
80% ethanolic extract of
Zingiber ofcinale
70% ethanolic extract of
Zingiber ofcinale
20% aqueous extract of
Zingiber ofcinale
Ethanolic extract of
Zingiber ofcinale
6-S 20mg/kg; given I.P. Renal ischemia-reperfusion in
6-S 5 or 10mg/kg; given
6-S 20mg/kg; given I.P. Cisplatin-induced renal injury in
8mg/kg daily; used for
42days
for 14weeks
100mg/kg;
administered for
16weeks
83days
administration at
300mg/kg
given orally for 83days
given orally for 83days
20weeks orally
2μg/h; bilateral
paraventricular nucleus
infusion for 28days
400 and 800mg/kg
given orally for 6 weeks
1g/kg/day; orally for
28days
125mg/kg; orally for 3
days
150mg/kg; orally for 3
weeks
I.P. for 2 weeks
Streptozotocin-induced DN
Kidney injuries in rats caused by
UUO
Streptozocin-induced DN in rats
Streptozocin-induced DN in rats
Male db/db diabetic mice
Streptozocin-induced DN in rats
Streptozocin-induced DN in rats
Spontaneously hypertensive rats
2K1C renovascular hypertensive
rats
Streptozocin-induced DN in rats
Streptozocin-induced DN in rats
Mercuric chloride-induced
kidney injury
Rat renal toxicity caused by lead
C57BL/6 male mice
Streptozocin-induced DN
C57BL/6 male mice
↓ TGF-β1, TSP-1, Grp78, CHOP
mRNA expression in kidney tissue
↓ p-PERK, p-elf2α and ATF-4
↓ MDA, Scr, BUN
↑ Nrf-2 and HO-1in kidney tissue
↓ MDA level
↑ SOD and CAT activities
↓ TGF-β1, α-SMA, and pSmad3
expression in kidney tissue
↓ Kidney/body weight, BUN, Scr,
and urinary protein levels over 24h
↑ p-AMPK/AMPK, P-ULK/ULK,
LC3-II/LC3-I, beclin-1 levels
↓ pmTOR/mTOR, TGF-β1, α-SMA
protein expression
↓ Scr, BUN, protein
↓ Expression levels of TGF-β,
vimentin, and α-SMA mRNA in
kidney tissue
↓ Drp1 expression and translocation
from cytoplasm to the mitochondria
↓ 24-h urinary protein, Scr, BUN
↓ IL-1β, IL-6, and MCP-1 levels in
kidney tissue
↓ TLR-4 protein level, p-IκBα/IκBα
ratio, and p-p65/p65 ratio
↓ MMP9, TIMP-1, TIMP-2, TGF-β1,
bronectin, and type IV collagen in
kidney
↑ MMP2 expression levels
↓ Hypertension
↓ Angiotensin II, aldosterone, IL-6,
IL-17, IL-23, osteopontin, and
KIM-1
↓ Mean arterial pressure
↓ NOX2, NOX4, Erk1/2, iNOS
↑ copper/zinc superoxide dismutase
levels in the paraventricular nucleus
↓ Scr, BUN, and MDA
↑ GSH level, SOD, CAT activity
↓ TNF-α, IL-6, IL-1β, cytochrome c,
caspase-3in kidney tissue
↓ MDA and TNF-α level
↑ TAC, SOD, CAT, Gpx activities
↑ Nrf-2 expression in renal tissue
↑ GSH level, SOD and CAT, GR,
GPx, and GST activities
↓ MDA level in renal tissue
↑ GSH level, GPx, GST, and catalase
activities in kidney tissue
↓ Scr, BUN
↓ mRNA expression of kidney
neutrophil gelatinase-associated
lipocalin, IL-6, MCP-1, MIP-2, KC
↑ HO-1 mRNA expression
↑ Nrf-2 mRNA expression
↓ Scr, BUN, MDA levels
↓ KIM-1, NGAL, NOX4, TNF-α,
IL-6, and MCP-1
↑ GSH level, SOD, and catalase
activities in kidney tissue
V. BaradaranRahimi and V. R. Askari
[21]
[22]
[27]
[29]
[30]
[28]
[31]
[32]
[33]
[34]
[40]
[41]
[42]
[43]
[44]
[45]
[46]
Role ofHerbal Medicines fortheTreatment ofChronic Kidney Disease
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(continued)
Table 1
Extract or constituent type Dose/concentration An overview of the study model Results References
6-G 10mg/kg; orally for 8
weeks
Streptozocin-induced DN in rats
↓ Levels of Scr, BUN, MDA, CRP,
IL-6 and 1β, and TNF-α
[47]
↑ GSH level
↑ SOD and CAT activities
6-G 100mg/kg; I.P. over 10
days
Gentamicin-induced kidney
injury
↓ Scr, BUN, MDA level
↑ GSH level
[48]
Improved pathological changes in
kidney tissue
6-G 50, 100, and 200mg/
kg; orally over 14
continuous days
6-G 50mg/kg; orally over 3
days
Carbendazim-induced kidney
damage in rats
Mercuric chloride-induced
kidney injury
↓ MDA and H
2O2
levels
↑ SOD and CAT activities
↑ GSH level in kidney tissue
↑ GSH level, SOD, catalase, GR,
GPx, and GST activities
[49]
[42]
↓ Kidney tissue MDA level
Punica granatum leaves
extract
50, 100, and 200mg/
kg; orally over 28days
Streptozocin-induced DN in rats
↓ Scr, BUN, urinary total protein,
urine volume, MDA
[55]
Improved histopathological changes
↑ GSH, catalase, and SOD activities
in renal tissue
A methanolic extract of
Punica granatum leaves
100, 200, and 400mg/
kg; taken orally for 8
weeks
Streptozocin-induced DN in rats
↓ Scr, BUN
↓ MDA level
↑ GSH level, CAT, and SOD
[56]
activities in renal tissue
A methanolic extract of
Punica granatum leaves
100, 200, and 400mg/
kg; taken orally for 8
weeks
Gentamicin-caused nephropathy
↓ Scr, BUN
↓ MDA and TNF-α level
↑ GSH level, catalase, and SOD
[57]
activities in renal tissue
PPEE 100mg/kg; orally over
2 weeks
Vancomycin-induced kidney
injury in rats
↓ MDA, C-reactive protein
↑ GSH level, catalase, and SOD
[58]
activities in the renal
↓ Caspase-3
↑ Bcl-2 renal expression
Punica granatum juice Administered orally for
10 weeks
CCl
-induced nephrotoxicity in
4
rats
↓ NO, and MDA level
↑ GSH level, CAT, SOD, GST, GPx
[59]
activities in kidney tissue
EA 50, 100, and 150mg/
kg; taken orally for 4
weeks
Induction of DN in rats by
streptozocin
↓ Scr, BUN, MDA, and TNF-α levels
↑ SOD activity in kidney tissue
↓ TLR-4, IRAK4, TRAF6, IKK-β,
[60]
NF-κBp65, and HMGB1 protein
expression in kidney tissue
EA Dosage of 10 and
30mg/kg; administered
orally over 21days
EA 20 and 40mg/kg daily;
orally over 14days
Rat renal injury caused by
sodium arsenite
Chronic renal failure caused by
5/6 nephrectomy
↓ Scr, BUN, MDA, and NO levels
↑ GSH level and SOD activity in
renal tissue
↓ Urine volume, urine protein, BUN,
Scr, MDA, TNF-α, IL-6, and
[61]
[62]
ICAM-1 level
↑ GSH level and SOD activity in
renal tissue
↓ miR-182, TGF-β1, bronectin, and
Bax expression levels
↑ FOXO3a and Bcl-2 expression
levels
EA 50, 100, and 150mg/
kg; given orally
Renal ischemic-reperfusion
injury in rats
↓ TNF-α, IL-1β, IL-6, MCP-1, MDA,
LDH, iNOS, COX-2 levels
[63]
↓ Bax and caspase-3 expression
↑ GSH level, SOD activity, and Bcl-2
expression in kidney tissue
↓ p-JAK1, p-JAK2, p-STAT1, and
NOX4 expression levels
297
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(continued)
Table 1
Extract or constituent type Dose/concentration An overview of the study model Results References
EA 10mg/kg, given I.P.,
EA 10mg/kg; orally taken
Vitis vinifera seed
proanthocyanidin extracts
Vitis vinifera seed
proanthocyanidin extracts
Vitis vinifera seed
proanthocyanidin extracts
Aqueous extracts of Vitis
vinifera fruits
V. vinifera seed extract 100mg/kg/day; orally
Curcuma longa 250mg/kg/day; orally
Curcumin 50, 100, and 200mg/
Curcumin 200mg/kg; orally for 6
Curcumin 100mg/kg; given orally
Curcumin Two doses of 20 and
Curcumin 300mg/kg/day; orally
Curcumin 100mg/kg; orally for 8
70% hydro-ethanolic
extract of Nigella sativa
over 8 weeks
for 7 days
250mg/kg/day; orally
for 16weeks
125 and 250mg/kg/
day; GSPE over 8
weeks
Oral administration of
200mg/kg for 28days
400mg/kg; given orally
over 4 weeks
over 8 weeks
for 8 weeks
kg; taken orally over
28days
weeks
over 8 days
40mg/kg; orally over
14 continuous days
over 30days
days
200 and 400mg/kg; I.P.
taken over 18days
Carbon tetrachloride-caused
kidney damage in rats
Nephrotoxicity caused by
amikacin in rats
Streptozotocin-induced DN in
rats
Streptozotocin-induced DN in
rats
Carboplatin and thalidomideinduced nephrotoxicity
Induction of DN by doxorubicin
in rats
Amiodarone-induced
nephrotoxicity in rats
Rats with kidney damage caused
by doxorubicin
The nephrotic syndrome
produced in rats by doxorubicin
Sodium arsenate-induced kidney
injury in mice
Gentamicin-induced
nephrotoxicity in rats
Potassium oxonate-induced
kidney inammation in mice
Passive Heymann nephritis in rats
Cisplatin-induced kidney damage
in rats
UUO in rats
↓ MDA level
↓ TNF-α, NF-κB, COX-2, and VEGF
↑ GSH level, CAT activity
↑ Nrf-2 expression in kidney tissue
↓ MDA, TNF-α, IL-6 levels, NF-κB,
and Bax expression
↑ GSH level, SOD, and CAT
activities
↓ GRP78, p-ERK and Caspase-12in
kidney tissue
↓ Scr, BUN, and MDA levels
↑ GSH level, SOD, and TAC
activities
↑ Nrf-2, HO-1, GST, and NQO1in
kidney tissue
↓ p53, TNF-α, and IL-6 expression
↓ MDA and NO levels
↑ GSH, GST, TAC levels
↑ SOD, CAT, and GPx activities
↓ Scr, BUN, and hs-CRP
↑ Nrf-2 mRNA expression in kidney
tissue
↓ Scr, MDA, and IL-6 levels
↑ SOD activity
↓ MCP-1 and TGF-β1 level
↓ Desmin, vimentin, and ED-1+ cells
immunostaining
↓ Urinary protein, MDA levels
↓ NF-κB p65 and Keap-1 expression
↑ HO-1, NQO-1, Nrf-2, IκBα
expression
↑ SOD activity
↓ IL-1β, IL-6, TNF-α, IFN-γ,
TGF-β1
↓ NF-κB
↓ P-JNK, P-ERK1/2, and P-p38
phosphorylation
↑ Nrf-2, NQO1, and HO-1 expression
↓ MDA and NO, IL-1β, IL-6, TNF-α
↑ SOD, CAT, and GSH-Px activities
↓ Caspase-3, and Bax
↑ Bcl-2
↓ IL-1β, NLRP3, ASC, and caspase1
expression
↓ Scr, BUN, and MDA levels
↑ GSH, SOD, CAT levels
↓ Bax, Caspase-3, p62, PI3K,
p-AKT, and p-mTOR expression
↑ Bcl-2, beclin1, Nrf-2, and HO-1
↓ Scr, BUN, MDA levels
↓ ERK1/2 phosphorylation
↓ NF-κB expression
↓ Bax/Bcl-2 ratio
↓ TNF-α, IL-6, KIM-1, and NGAL
↑ GSH level
↑ IL-10 mRNA expression in kidney
tissue
↓ Angiotensin II, MCP-1, MDA, and
TNF-α levels
↑ GSH level, SOD, and catalase
activities in kidney tissue
V. BaradaranRahimi and V. R. Askari
[64]
[65]
[67]
[68]
[69]
[70]
[71]
[75]
[76]
[77]
[78]
[79]
[80]
[81]
[92]
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(continued)
Table 1
299
Extract or constituent type Dose/concentration An overview of the study model Results References
Nigella sativa 1g/kg/day; orally for
10 days
Radiation-induced kidney injury
in rats
↓ Total oxidant status and lipid
hydroperoxide levels
[93]
↑ Total anti-oxidant status
↑ Paraoxonase and ceruloplasmin
activities in kidney tissue
Nigella sativa oil and
thymoquinone
Aqueous extract of
Rosmarinus ofcinalis
2mL/kg; orally
1.5mg/kg; orally
over 34days
100mg/kg; taken orally
for 14days
Cisplatin-induced kidney injury
in rats
Carbon tetrachloride-induced
nephropathy in mice
↓ Scr, BUN, and MDA level
↑ GSH level
↑ SOD, CAT, GPx, and GR activities
↓ Scr, BUN, LDH, MDA
↑ GPx and GSH levels
[94]
[100]
↑ SOD and CAT activities in kidney
tissue
Rosmarinus ofcinalis
essential oil
0.02% v/w; orally for
60days
Diethylnitrosamine-induced renal
injury in rats
↓ Urea, Scr, and MDA levels
↑ Total anti-oxidant concentration,
[101]
CAT, GPx activities improved
histopathological changes
Rosmarinus ofcinalis
essential oil
0.5mL/kg; orally over
14days
Potassium dichromate-induced
kidney injury in rats
↓ Urea, creatinine, uric acid, MDA,
and H
2O2
levels
[102]
↑ GSH level, SOD, catalase, GPx,
and GST activities
Improved histological changes
Rosmarinic acid 5, 10, 20mg/kg; given
orally over 8 days
Kidney damage caused by
cisplatin in mice
↓ MDA, NO levels
↓ IL-1β, IL-6, and TNF-α
[103]
↑ SOD, CAT activities, GSH, and
TAC levels in kidney tissue
↓ Keap-1in kidney tissue
Rosmarinic acid 25–100mg/kg; taken
orally over 28days
Chlorpyrifos-induced kidney
injury in rats
↓ Urea, Scr, KIM-1, ROS, MDA,
NO, IL-1β, TNF-α, and NF-κB p65
[104
]
↑ GSH, SOD, and CAT activities
↓ Bax, caspase-3, Keap-1
↑ Renal Bcl-2, Nrf-2, HO-1 and
SIRT1
Rosmarinic acid 25mg/kg; given orally
over 60days
Chromium-induced kidney injury
in rats
↓ MDA level
↑ GSH level
[105]
↑ Nrf-2 mRNA level
Rosmarinic acid 50mg/kg; taken orally
over 14days
Cadmium-induced nephrotoxicity
in mice
↓ CRP, IL-1β, IL-6, TNF-α, ROS,
NO, H
, and MDA levels
2O2
[106]
↑ GSH, GPx, and GR levels
↑ SOD and CAT activities
↓ Caspase-3, caspase-8, caspase-9,
NF-κB, PKC, TNFR, TGF-β1,
SMAD3, and α-SMA expression
levels in kidney tissue
Huangkui capsule (HKC), diabetic nephropathy (DN), intraperitoneal (IP), salvianolic acid A (SAA), salvianolic acid B (SAB), 6-shogaol (6-S),
6-gingerol (6-G), Ellagic acid (EA), blood urea nitrogen (BUN), uric acid (UA), malondialdehyde (MDA), 8-hydroxy-2′-deoxyguanosine
(8OhDG), superoxide dismutase (SOD), Interleukin (IL), creatinine (Cr), mammalian target of rapamycin (mTOR), transforming growth factor-β1
(TGF-β1), nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4), tumor necrosis factor-α (TNF-α), α-smooth muscle actin (α-SMA),
nuclear factor erythroid-2-related factor 2 (Nrf-2), phosphorylation-extracellular signal-regulated kinase (p-ERK), heme oxygenase-1 (HO-1),
kelch-like ECH-associated protein 1 (Keap-1), bone morphogenetic protein 7 (BMP-7), NAD(P)H quinone dehydrogenase 1 (NQO1), α-smooth
muscle actin (α-SMA), nuclear factor-κB (NF-κB), glutathione peroxidase (GPx), catalase (CAT), p38 mitogen-activated protein kinase (MAPK),
p-glycogen synthase kinase-3β (p-GSK-3β), intercellular adhesion molecule-1 (ICAM-1), minimal change disease (MCD), vascular cell adhesion
molecule-1 (VCAM-1), angiopoietin-like 4 (Angptl4), broblast growth factor-2 (FGF-2), glutathione (GSH), thrombospondin-1 (TSP-1),
glucose- regulated protein 78 (Grp78), activating transcription factor (ATF)-4, phosphorylated eukaryotic initiation factor 2 alpha (p-elf2α), phosphorylated Smad3 (pSmad3), dynamin-related protein 1 (Drp1), kidney-injury-molecule (KIM-1), inducible nitric oxide synthase (iNOS),
glomerular ltration rate (GFR), matrix metallopeptidase (MMP), tissue inhibitor matrix metalloproteinase (TIMP), reactive oxygen species
(ROS), macrophage inammatory protein-2 (MIP-2), TNF Receptor Associated Factor 6 (TRAF6), AMP-activated protein kinase (AMPK), keratinocyte chemoattractant (KC), glutathione reductase (GR), glutathione-S-transferase (GST), nitric oxide (NO), Interleukin-1 receptor-associated
kinase 4 (IRAK4), inhibitor of nuclear factor kappa-B kinase (IKK-β), vascular endothelial growth factor family (VEGF), high mobility group box
1 (HMGB1), Interferon gamma (IFN-γ), neutrophil gelatinase-associated lipocalin (NGAL), Sirtuin 1 (SIRT1), protein kinase C (PKC), tumor
necrosis factor receptor (TNFR)
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