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Received: 25 September 2020    Revised: 17 February 2021    Accepted: 21 February 2021

DOI: 10.1111/jfbc.13687

FULL ARTICLE

Protective effects of Dendrobium candidum Wall ex Lindl. on

high-­fat diet-­induced liver damage in mice

Xiong-­Zhang Yin1 | Wei-­Ming Chi2 | Ling Zhang3 | Yan-­Qi Su4 | Zhong-­Yuan Zhang5 |

Cheng-­Bin Xue6

1
Department of Pharmacy, Tongji Hospital
Affiliated to Tongji Medical College Abstract
Huazhong University of Science and D. candidum Wall. ex Lindl. (D. candidum) is a traditional Chinese herbal medicine with
Technology, Wuhan, China
2 multiple therapeutic properties. D. candidum was administered to mice with high-­fat
Department of Pharmacy, The Third
People's Hospital of Hubei Province, Wuhan, diet (HFD)-­induced nonalcoholic fatty liver disease (NAFLD) and its mechanism of
China
action was elucidated. D. candidum was intragastrically administered to HFD mice
3
Department of Pharmacy, The First
People's Hospital of Xiantao, Xiantao, China
for 6 weeks at a dosage of 200 or 400 mg/kg. D. candidum reduced body weight gain
4
Department of Pharmacy, Wuhan Caidian and blood glucose levels in HFD mice in a dose-­dependent manner, while significantly
District People's Hospital, Wuhan, China reducing lipid accumulation in the liver. D. candidum significantly regulated the ex-
5
Department of Pharmacy, Affiliated
pression of lipid metabolism-­and gluconeogenesis-­related genes and inhibited acti-
Tianyou Hospital Wuhan University of
Science and Technology, Wuhan, China vation of the NLRP3 inflammasome. In summary, D. candidum significantly inhibits fat
6
Department of Pharmacy, Huazhong accumulation, maintains lipid metabolism and glucose homeostasis, and inhibits the
University of Science and Technology
Hospital, Wuhan, China inflammatory response in the liver of HFD mice. Our findings suggest that D. candi-
dum may be an effective therapeutic strategy against NAFLD injury.
Correspondence
Cheng-­Bin Xue, Huazhong University of Practical applications
Science and Technology Hospital, 1037
The occurrence and development of fatty liver is closely related to abnormalities in
Luoyu Road, Hongshan District, Wuhan City,
Hubei Province, China. lipid and glucose metabolism. An HFD-­induced NAFLD mouse model was used to
Email: chengbin027@yeah.net
study the effects of D. candidum. After treatment with D. candidum, lipid and glucose
metabolism in the mice was effectively regulated, which reduced liver damage and
fat storage with obvious protective effects on the liver. Our results suggest that D.
candidum has potential for further clinical application in the treatment of NAFLD.

KEYWORDS

Dendrobium candidum, lipid metabolism, NLRP3, nonalcoholic fatty liver disease

1 |  I NTRO D U C TI O N been increasing continuously (Zhou et al., 2019). Therefore, efforts

Lifestyle changes in modern society has led to higher consumption
of high-­fat and high-­cholesterol foods. The incidence of nonalco-
holic fatty liver disease (NAFLD) is increasing, and the age of onset is
reducing. Approximately 25%–­45% of adults worldwide are affected
by NAFLD (Bellentani et al., 2010); NAFLD has become the first liver
disease to occur in developed countries. In China, it is the second-­
most common liver disease after viral hepatitis and its incidence has
must be made to reduce the burden of NAFLD.
NAFLD is characterized by abnormal lipid accumulation in he-
patocytes (Boutari et al., 2018). Studies have revealed that being
overweight, oxidative stress, and insulin resistance are the main
causes of NAFLD (Gomaraschi et al., 2019; Rives et al., 2020). NAFLD
can progressively develop into cirrhosis and subsequently into he-
patocellular carcinoma. The incidence of cirrhosis in patients with
NAFLD occurring within 10 years of onset is as high as 25% (Bhagat

J Food Biochem. 2021;45:e13687. wileyonlinelibrary.com/journal/jfbc |

© 2021 Wiley Periodicals LLC.     1 of 10
https://doi.org/10.1111/jfbc.13687
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2 of 10       YIN et al.
et al., 2010). However, the pathological mechanism of NAFLD is still
poorly understood. NAFLD is the result of a wide range of patho-
logical factors. Recent research has revealed potential lipid metab-
olism disorders, insulin resistance, and cytokine-­
related damage
mechanisms in the pathogenesis of NAFLD (Shoreibah et al., 2016;
Wallace et al., 2018). Abnormal lipid metabolism is considered to be
one of the most critical pathogenic links in NAFLD. Abnormal lipid
metabolism and other factors induce Kupffer cells to get activated
and release inflammatory mediators, which is an important process
that bridges fatty liver and nonalcoholic steatohepatitis (NASH), and
is also a key factor in the induction of progressive liver fibrosis (Mato
et al., 2019).
The effective prevention or treatment of NAFLD injury has
become a hot topic in the study of hepatic injury. However, cur-
rently, there are few effective preventive measures or treatment
options for NAFL injury. The commonly used insulin sensitizers,
lipid-­lowering drugs, and antioxidant stress relievers are limited
by adverse side effects or a lack of clinical data proving their effi-
cacy (Ali & Cusi, 2009). In addition to lifestyle changes, increasing
evidence shows that the supplementation of functional nutrients
is an indispensable and effective means of preventing the oc-
currence and development of NAFL injury. Traditional Chinese
medicine has good prospects for the prevention and treatment
of liver injury (Melchart et al., 2017). Dendrobium candidum Wall
ex Lindl. (D. candidum) is a subspecies of the Dendrobium family.
Dendrobium candidum has long been used as a traditional Chinese
herb drug (Wang et al., 2014). It has a broad range of biological
functions, including anticancer activity (Li, Sun, Zhou, et al., 2014),
osteoprotection (Wang et al., 2018), and inflammatory regulation
effects (Gong et al., 2020). Recent studies also reveal the hepatic
therapeutic effect of D. candidum (Li, Sun, Wang, et al., 2014). In
this study, D. candidum was utilized as a treatment for mice with
high-­f at diet-­induced NAFLD. Through intragastric administration,
the protective effect of D. candidum on liver function and injury
was investigated, providing scientific information for further ex-
ploration of the mechanisms underlying NAFLD and a reference
for the clinical administration of D. candidum.
2 |  M ATE R I A L S A N D M E TH O DS
2.1 | Animals
Forty-­t welve-­week-­old male C57BL/6 mice were provided by the
Laboratory Animal Center of Huazhong University of Science and
Technology (SCXK (E) 2016–­0 009). All experimental procedures
were approved by the Institutional Animal Care and Use Committee
at Huazhong University of Science and Technology, and all meth-
ods were performed in accordance with the relevant guidelines
and regulations. A mouse model of NAFLD was developed as pre-
viously reported (Hong et al., 2020). Briefly, the mice in the control
group (Con) were fed a normal standard diet (33% protein; 58%
carbohydrate; 9% fat) (#V1535, Ssniff, Soest, Germany) and those
in the HFD group were fed a 60% kcal high-­fat diet (HFD) (20%
protein; 20% carbohydrate; 60% fat) (#D12492, Research Diets,
New Brunswick, NJ, USA) for a period of 12 weeks. After 6 weeks
of feeding with the HFD, the HFD mice were randomly divided
into three groups: a nontreated control group (HFD group) and
two D. candidum-­t reated groups (200 or 400 mg/kg body weight
of the aqueous extract). Each group contained 10 mice. Treatment
groups were treated with once-­daily intragastric administration of
D. candidum solution. D. candidum (Shanghai Pharmacy Co., Ltd.,
Shanghai, China) freeze-­
dried powder was mixed with 20-­
fold
volume of water and was boiled; the extracted samples were col-
lected after stirring overnight. The D. candidum groups received
200 or 400 mg/kg body weight of the aqueous extract intragastri-
cally (Li, Sun, Wang, et al., 2014). The control group received an
intragastric administration of water. Isoflurane was used for anes-
thesia and the mice were sacrificed for tissue collection. We meas-
ured the body weight and food intake of the mice every week.
Blood glucose levels were measured monthly using a One-­Touch
Ultra glucometer (Lifescan, Milpitas, CA, USA) at the same time
of the day.
2.2 | Histopathological observation
Following overnight fixation in 4% paraformaldehyde, the embedded
liver tissues were sliced into 4-­mm sections using a Leica automatic
microtome (Leica Microsystems, Wetzlar, Germany) and stained with
hematoxylin and eosin (H & E) and 0.3% Oil Red O in isopropanol
for histological assessment under light microscopy (Olympus BX51,
Tokyo, Japan).
2.3 | Blood biochemistry
At the end of the intervention, mice were anesthetized and orbital
sinus bleeding was performed by removing the eyeball. Blood was
collected for assessments of serum alanine aminotransferase (ALT),
aspartate transaminase (AST), and cholesterol (CHOL) using an au-
tomatic biochemistry analyzer. Serum insulin and hepatic IL-­6 and
TNF-­α levels were determined using an enzyme-­linked immuno-
sorbent assay (ELISA) kit (Millipore, Bedford, MA, USA). The ho-
meostasis model insulin resistance index was calculated as follows:
homeostasis model insulin resistance assessment (HOMA-­IR) = [FBG
(mmol/L) × FINS (mIU/L)]/22.5.
2.4 | Quantitative real-­time polymerase chain
reaction (qRT-­PCR)
Total RNA was isolated using TRIzol and transcribed into complemen-
tary DNA using the RevertAid First Strand cDNA Synthesis Kit (Thermo
Fisher Scientific, Inc., Waltham, MA, USA). Then, qRT-­PCR was carried
out using the QuantiNova™ SYBR® Green PCR kit. GAPDH was used
YIN et al.
as the internal standard. The primer sequences used were as follows:
FAS, 5-­GCCATGCCCAGAGGGTGGTT-­3, 3-­AGGGTCGACCTGGTC CT
CA-­5; SREBP1, 5-­GAAGCTGTCGGGGTAGCGTC-­3, 3-­CTCTCAGGA
GAGTTGGCACCTG-­5; G6P, 5-­GTGCCTGTCCGTCGGGA TGT-­3; 3-­G
TGAG CTCGGTGACGGTCTC-­5; PCK1, 5-­ATCTTTGGTGGCCGTAGA
CCT-­3; and 3-­CCGAAGTTGTAGCCGAAGAA-­5′.
2.5 | Glucose tolerance test
Oral glucose tolerance tests (OGTT) (Day et al., 2009) were per-
formed for 48 hr after the indicated time and mice were fasted for
12 hr followed by oral glucose gavage (2.0 g/kg body weight). Blood
glucose was measured by collecting blood from the tail veil at 0, 60,
120, and 180 min after glucose stimulation.
2.6 | Immunohistochemistry
After fixation with 4% paraformaldehyde, permeabilization with
0.2% Triton X-­
100, and blocking with 5% BSA, cross sections
were incubated with primary antibodies anti-­IL-­6 (1:500, ab6672,
Abcam, Cambridge, MA, USA), anti-­
TNF-­
α (1:400, ab11564,
Abcam), or anti-­NLRP3 antibody (1:800, ab4207, Abcam) at 4°C
overnight. After three washes with 0.01 M PBS (5 min each), a
secondary antibody was added to the sections for a 30-­min incu-
bation at 37°C, followed by five PBS washes. Thereafter, the sec-
tions were incubated with HRP-­labeled avidin for 30 min at 37°C
and reacted with DAB.
2.7 | Western blotting
The samples were mixed with gel-­loading dye, boiled at 95°C for
5 min, and then subjected to separation by SDS-­PAGE on a 15%
polyacrylamide gel. After SDS-­
PAGE, the proteins were trans-
ferred onto a PVDF membrane. The membrane was blocked with
5% skim milk overnight after the blotting procedure. Primary anti-
bodies against NLRP3 (1:2,000, ab4207, Abcam), ASC1 (1:3,000,
ab228630, Abcam), cleaved Caspase-­
1 (1:2,000, 89332S, Cell
Signaling Technology, Danvers, MA, USA), IL-­1β (1:3,000, 31202S,
Cell Signaling Technology), and GAPDH (1:1,000, G9545, Sigma, St.
Louis, MO, USA) were diluted 1:1,000 in 5% skim milk and incubated
with the membranes for 2 hr at room temperature. Then, the mem-
brane was washed with TBST three times, followed by incubation
with the secondary antibody at 1:1,000 dilution for 1 hr at 25°C.
After washing with TBST three times, the signals were detected
using Amersham ECL Prime western blotting Detection Reagent (GE
Healthcare, Buckinghamshire, UK). The chemiluminescent signal was
recorded using the ChemiDoc™ XRS + System and analyzed using
the Image Lab™ Software (Bio-­Rad Laboratories, Hercules, CA, USA).
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2.8 | Statistical analysis
Results were expressed as the mean ±  SEM and analyzed using
SPSS 22.0 (SPSS, Inc.). The significance of differences was ana-
lyzed using Student's t-­
test or one-­
way analysis of variance
(ANOVA). p < .05 was considered to indicate a statistically signifi-
cant difference.
3 | R E S U LT S
3.1 | D. candidum produces metabolic changes and
alters liver histopathology in HFD-­fed mice
D. candidum was administered intragastrically to investigate its
effect on NAFLD in HFD-­fed mice. D. candidum prevented the
excessive weight gain produced by HFD in a dose-­d ependent man-
ner (Figure 1a). At the end of 12 weeks, the mean body weight
for each group is 27.28 ± 3.46, 36.85 ± 4.21, 31.46 ± 6.31, and
28.53 ± 2.86 correspondingly. We assessed the glucose metabolic
parameters of fasting blood glucose (FBG). The FBG of the HFD
mice reached over 15 mmol/L, while D. candidum treatment res-
cued glucose regulation, with a dose-­d ependent decrease in FBG
levels (Figure 1b). We compared the appearance of liver samples
at the end of the intervention. Morphologically, the livers in the
HFD group were enlarged compared with those in the normal
diet control group. The D. candidum-­supplemented HFD groups
displayed slightly smaller and less discolored livers than the HFD
group. Larger lipid droplets in the liver were observed in HFD-­
fed mice by H&E and Oil Red O staining microscopic images but
were largely disseminated after treatment with D. candidum in a
dose-­d ependent manner (Figure 1c,d). These data suggest that D.
candidum lowered lipid accumulation in liver tissue in the HFD-­fed
group.
3.2 | Effect of D. candidum on liver damage and
glycometabolism in HFD-­fed mice
To further investigate the protective role of D. candidum in liver
tissue, we evaluated serum parameters. Levels of serum aspartate
transaminase (AST), alanine aminotransferase (ALT), and cholesterol
(CHOL), which were elevated in the HFD-­fed mice, were reduced by
D. candidum treatment in a dose-­dependent manner (Figure 1a–­c).
After the treatment, D. candidum also reduced basal glucose levels
measured before glucose loading. In the OGTT, 400 mg/kg D. candi-
dum treatment caused a significant decrease in glycemia (Figure 2d)
and insulin levels (Figure 2e) at 120 min. Accordingly, IR assessed by
the HOMA index was markedly reduced by 400 mg/kg dose of D. can-
didum (Figure 2f). The HOMA index for each group is 52.54 ± 11.43,
95.23 ± 14.85, 83.13 ± 9.57, and 73.43 ± 8.97 correspondingly.
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F I G U R E 1   Effect of D. candidum on metabolic changes and hepatic histopathology in HFD-­fed mice. (a) Body weight in each group
indicated (n = 10 in each group). (b) Fasting blood glucose level in each group indicated (n = 10 in each group). (c) Representative pictures of
the liver HE staining of mice in each group indicated. Scale bar = 100 μm. (d) Representative pictures of the liver Oil Red O staining of mice
in each group indicated. Scale bar = 100 μm. The values are expressed as Mean ± SEM, ###p < .001 versus Con; **p < .01; ***p < .001 versus
HFD

3.3 | D. candidum rescues expression of genes
involved in glucose and lipid metabolism
To investigate the lipogenic inhibition mechanism of D. candidum, we
first examined the expression of genes involved in lipid metabolism.
SREBP1 activation of FAS is an important pathway for lipid synthesis,
and the expression of FAS and SREBP1 was significantly increased in
the liver of HFD mice. In contrast, D. candidum decreased mRNA lev-
els of FAS and SREBP1 in a dose-­dependent manner, indicating that
D. candidum could regulate lipid synthesis (Figure 3a,b). The expres-
sion of FAS is 462.64 ± 44.43% for HFD group, 320.32 ± 44.43%
for 200 mg/kg dose, and 167.56 ± 23.53 for 400 mg/kg dose
YIN et al. |
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F I G U R E 2   Effect of D. candidum on hepatic damage and glucose homeostasis in HFD-­fed mice. Serum AST (a), ALT (b), and CHOL(c)
levels were measured with the corresponding commercial kits (n = 6, each group). OGTT glycemia (d), insulin levels (e), and HOMA IR (f) were
also reported (n = 6 in each group). The values are expressed as Mean ± SEM. ##p < .01; ###p < .001 versus Con; *p < .05, **p < .01 versus
HFD

correspondingly. We further examined the expression of genes (Figure 3c,d). The expression of PCK1 is 401.77 ± 32.86% for HFD
involved in hepatic glucose metabolism. Expression levels of glu- group, 263.53 ± 36.64% for 200 mg/kg dose, and 145.54 ± 31.77
coneogenic genes (G6P, PCK1) in liver tissue were decreased by for 400 mg/kg dose correspondingly. These results suggested that
D. candidum administration in HFD mice in a dose-­dependent manner D. candidum decreases hepatic lipid synthesis and gluconeogenesis.
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6 of 10       YIN et al.

F I G U R E 3   D. candidum rescue genes expression involved in glucose and lipid metabolism. Expression of lipid metabolism genes (A and
B) and glucose metabolism genes (C and D) in the livers of mice in each treatment group. The values are expressed as Mean ± SEM (n = 6 in
each group). ###p <.001 versus Con; *p <.05; **p <.01; ***p <.001 versus HFD

3.4 | D. candidum treatment counteracts hepatic
inflammation
IL-­6 and TNF-­α are important proinflammatory mediators involved in
liver damage. As shown in Figure 4a,b, the HFD induced an increase in
IL-­6 and TNF-­α levels compared to those in the control group, and this ef-
fect was alleviated by D. candidum treatment in a dose-­dependent man-
ner. This anti-­inflammatory effect of D. candidum was confirmed by the
hepatic ELISA results for IL-­6 and TNF-­α concentrations (Figure 4c,d).
The mean TNF-­
α concentrations for each group is 16.68 ± 6.43,
67.32 ± 11.63, 51.12 ± 7.27, and 38.53 ± 7.12 correspondingly.
We first detected the expression of NLRP3 inflammasome compo-
nents (including NLRP3, ASC, caspase-­1, and IL-­1β) in the mice. The
expression of NLRP3, ASC1, cleaved Caspase-­1, and IL-­1β increased
more than four times in HFD-­fed mouse liver tissue; however, the
expression of these NLRP3 inflammasome-­associated pathways de-
creased in a dose-­dependent manner after D. candidum treatment
(Figure 5a–­e). The expression of IL-­1β is 431.12 ± 43.18% for HFD
group, 365.97 ± 54.24% for 200 mg/kg dose, and 177.86 ± 28.43 for
400 mg/kg dose correspondingly. The NLRP3-­positive cells in the
liver further validated this observation (Figure 5f). These results dem-
onstrate that D. candidum can alleviate HFD-­induced hepatic injury
possibly by the inhibition of NLRP3 inflammasome activation.

3.5 | D. candidum inhibits the activation of the

NLRP3 inflammasome in the liver of the HFD mouse 4 | D I S CU S S I O N

Finally, we investigated whether the effect of D. candidum on liver dam- The onset of NAFLD is accompanied by a variety of pathological
age was associated with the inhibition of the NLRP3 inflammasome. processes (Newton, 2010), and current treatments mainly involve
YIN et al. |
      7 of 10

F I G U R E 4   Effect of D. candidum on the production of pro-­inflammatory cytokines in HFD-­fed mice. (a) Representative
immunohistochemical staining showing the expression of IL-­6 (a) and TNF-­α (b) at liver. The effect of D. candidum on (a) IL-­6 and (b) TNF-­α
levels in liver was measured by ELISA. The values are expressed as Mean ± SEM. (n = 8 in each group). ##p < .01; ###p < .001 versus Con;
*p < .05; **p < .01; ***p < .001 versus HFD

lifestyle interventions, such as dietary energy restriction and exer-
cise (Ali & Cusi, 2009). However, this type of treatment is difficult to
maintain and the control process of the disease is passive; therefore,
there is an urgent need to develop new drugs to treat NAFLD. In
this study, we established a mouse NAFLD model using HFD. Our
experimental results showed that D. candidum could significantly
reduce body weight, blood glucose level, and liver lipid accumula-
tion in HFD-­fed mice. We also found that lipid metabolism, gluco-
neogenesis, and NLRP3 inflammasome-­related pathway alterations
were involved in the therapeutic effect of D. candidum. Our study
reveals the protective role of D. candidum in NAFLD and its potential
mechanism in improving liver fat metabolism, insulin resistance, and
inflammation.
In the drug therapy of NAFLD, in addition to traditional drug
choices, special functional components found in food can prevent
and improve NAFL injury, which is of great significance in improv-
ing the quality of life of individuals with NAFL injuries (Westfall
et al., 2020) (Jacome-­Sosa et al., 2014). Previous studies have found
that D. candidum has many bioreactive effects. D. candidum can
exert an anticancer role in a variety of cancers, such as liver can-
cer (Guo et al., 2019), breast cancer (Sun et al., 2016), and colon tu-
mors (Zhao et al., 2014). D. candidum has also shown target organ
protective roles under pathophysiological conditions such as in the
kidney (Chang et al., 2019) and salivary glands (Xiao et al., 2011).
Additionally, D. candidum significantly prevents liver damage in
hyperuricemic rats (Lou et al., 2020). Li, Sun, Wang, et al. (2014)
showed that D. candidum could attenuates CCl4-­induced liver dam-
age in mice. However, the effect of D. candidum on NAFLD has not
been reported. In our study, we found that D. candidum significantly
improves hepatic function in HFD mice. Our histopathological ev-
idence showed changes in fat metabolism; therefore, we studied
the expression of adipose metabolism-­and gluconeogenesis-­related
genes in mouse liver by qRT-­PCR. SREBP1-­FAS is a key pathway
of lipid synthesis in the liver (Chen et al., 2020). The reduction in
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8 of 10       YIN et al.

F I G U R E 5   D. candidum attenuates the activation of the NLRP3 inflammasome induced by a high-­fat diet mouse model. (a–­e) Western
blots of NLRP3, ASC, Cleaved Caspase-­1, and IL-­1β were performed with liver tissues. (f) The immunohistochemistry staining of NLRP3
inflammasome was significantly decreased in liver tissues of the HFD-­D. candidum. The values are expressed as Mean ± SEM (n = 6 in each
group). ###p < .001 versus Con; *p < .05; **p < .01; ***p < .001 versus HFD

SREBP1-­
FAS expression should be implicated in the effect of
D. candidum in regulating lipid synthesis after HFD in mice. In addi-
tion, the glycolysis-­related genes G6P and PCK1 were inhibited by
D. candidum. These results reveal the mechanisms by which D. can-
didum can reduce hepatic gluconeogenesis and lipid synthesis.
NAFLD is a complex inflammatory process that mediates the
progress of hepatocyte steatosis to steatohepatitis. The NLRP3
inflammasome plays an important role in liver steatosis, inflamma-
tion, liver injury, and fibrosis (Shao et al., 2015). The NLRP3 inflam-
masome can be seen not only in immune cells, such as Kupffer cells,
neutrophils, and dendritic cells, but also in some nonimmune cells,
such as hepatocytes, hepatic stellate cells, endothelial cells, and my-
ofibroblasts (Wree et al., 2014). In Kupffer cells, selective reduction
in the release of IL-­1 α can reduce the expression of cytokines in
the liver, and activation of the NLRP3 inflammasome is involved in
the coordination of Kupffer cells (Olteanu et al., 2014). In the NASH
mouse model induced by a long-­term high-­fat diet, caspase-­1 mRNA
and serum IL-­1β levels of NLRP3 inflammasome are significantly in-
creased (Mridha et al., 2017), and this was consistent with our results.
These results suggest that the NLRP3 inflammasome is involved in
the development of NAFLD. However, no definite target drug of
NLRP3 could be used. Our results showed that D. candidum reduced
NLRP3 inflammasome activation induced by HFD and decreased IL-­
1β or caspase-­1 and ASC production in the liver. Our results demon-
strate that D. candidum is a pharmacological inhibitor of the NLRP3
inflammasome and alleviates the NLRP3 inflammasome activation
of NAFLD in vivo. There has been no research demonstrating the ef-
fects of D. candidum on inhibiting NLRP3 inflammasome-­dependent
cell or tissue damage. In future, we plan to further investigate the
mechanism by which D. candidum inhibits the NLRP3 inflammasome.
In conclusion, our results showed that D. candidum can signifi-
cantly inhibit lipid accumulation, maintain lipid metabolism and
YIN et al.
glucose homeostasis, and inhibit NLRP3 inflammatory responses
in the liver of the HFD mice and the possible mechanism of action
has been elucidated. The pharmacodynamic mechanisms of D. can-
didum against NAFLD have multiple therapeutic effects on multiple
targets, suggesting the feasibility of treatment for NAFLD. Our re-
search provides new treatment options for NAFLD.
C O N FL I C T O F I N T E R E S T
The authors declare that they have no competing interests.
C O N S E N T FO R P U B L I C AT I O N
All authors agreed to the publication of this study.
AU T H O R C O N T R I B U T I O N
Xiongzhang Yin: Formal analysis; Investigation. Wei-­Ming Chi:
Investigation; Validation. Ling Zhang: Software; Supervision. Yan-­Q i
Su: Data curation; Validation. Zhong-­Yuan Zhang: Methodology;
Project administration. Chengbin Xue: Conceptualization;
Investigation.
DATA AVA I L A B I L I T Y S TAT E M E N T
The datasets used or analyzed during the current study are available
from the corresponding author upon reasonable request.
ORCID
Cheng-­Bin Xue  https://orcid.org/0000-0002-1097-5149
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How to cite this article: Yin X-­Z, Chi W-­M, Zhang L, Su Y-­Q,
Zhang Z-­Y, Xue C-­B. Protective effects of Dendrobium
candidum Wall ex Lindl. on high-­fat diet-­induced liver damage
in mice. J Food Biochem. 2021;45:e13687. https://doi.
org/10.1111/jfbc.13687