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Exploring Natural Products as Modulators of Oxidative Stress in Health...
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Exploring Natural Products as Modulators of Oxidative Stress in Health and Disease

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: closed (25 October 2024) | Viewed by 3330

Special Issue Editors

Dr. Antonella Di Sotto

E-Mail Website
Guest Editor
Department of Physiology and Pharmacology “V. Erspamer”, Sapienza University of Rome, Rome, Italy
Interests: natural substances; herbal extracts; waste; plant phytocomplexes; polyphenols; terpenoids; cancer chemoprevention; chemoresistance; STAT3; Pgp; Nrf2; DNA-damage; metabolic reprogramming; autophagy; genoprotection; hypoglycemic activity; antiglycative properties; antioxidant defenses; antiviral herbal extracts; inflammation; immunomodulation
Special Issues, Collections and Topics in MDPI journals
Dr. Silvia Di Giacomo

E-Mail Website
Guest Editor
Unit of Human Nutrition and Health, Department of Food Safety, Nutrition and Veterinary Public Health, National Institute of Health, Rome, Italy
Interests: natural products; terpenoids; polyphenols; chemoprevention; hepatocellular carcinoma; multidrug resistance; ABC-transporters; Nrf2; epithelial–mesenchymal transition (EMT)
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In recent years, natural products have become increasingly popular due to the wide range of biological activities ascribed to them. In particular, their ability to modulate oxidative stress, which plays a pivotal role in the development and progression of several pathologic conditions (e.g., neurodegeneration, cardiovascular diseases, metabolic ailments, diabetes mellitus, aging, and cancer), has been proposed as a potential strategy via which to promote human health.

Since the complete avoidance of the factors that trigger oxidative stress is not feasible, enhancing the cellular antioxidant system by using natural products could represent an alternative technique able to tackle this problem. Epidemiological studies have demonstrated an association between natural antioxidants and human health, suggesting that they are mainly effective in counteracting non-communicable diseases, such as neurodegenerative and cardiovascular diseases, diabetes, and cancer.

However, from the other side, overexposure to natural antioxidants can also lead to adverse effects, especially in highly susceptible people, such as cancer patients. Moreover, other adverse reactions may occur as a consequence of polymorphisms, concomitant pathologies, or pharmacological treatments. In this scenario, it is of the outmost importance to elucidate the role of natural products in oxidative stress modulation, in order to better harness their benefits while avoiding the possible risk of toxicity.

In line with this evidence, the aim of this Special Issue is to collect original articles and review papers focused on unveiling the dual antioxidant or pro-oxidant role of natural products and the possible pharmaceutical applications and safety.

The scope of this Special Issue includes, but is not limited to, the following:

  • discovering novel sources of antioxidants, with a special focus on chemically characterized extracts from medicinal plants, waste materials, and innovative plant production;
  • investigating the role of antioxidant agents in countering various pro-oxidant stressors and their effectiveness in experimental models of inflammatory and oxidative-related diseases;
  • unravelling the mechanism underlying the potential adverse reactions associated with antioxidant agents;
  • exploring the effects on cell signaling pathways and molecular targets;
  • carrying out pharmacokinetic and digestion studies to better understand the absorption and metabolism of antioxidants;
  • clarifying the safety and efficacy of antioxidants in clinical trials.

Special attention will be devoted to papers addressing the role of antioxidants in cancers (e.g., Nrf2 modulators) and in liver damage. Papers presenting pharmaceutical formulations that are able to improve the bioavailability and delivery of antioxidants to targets are also welcome.

Dr. Antonella Di Sotto
Dr. Silvia Di Giacomo
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pharmaceuticals is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • plant-based herbal extracts
  • waste
  • natural substances
  • medicinal plants
  • food supplements
  • liver
  • cancer
  • noncommunicable diseases
  • chemoprevention
  • molecular mechanisms
  • adverse reactions
  • safety

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Published Papers (3 papers)

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22 pages, 7927 KiB  
Article
Chemical Investigation and Regulation of Adipogenic Differentiation of Cultivated Moringa oleifera
by Duc Dat Le, Eunbin Kim, Thinhulinh Dang, Jiseok Lee, Choon Ho Shin, Jin Woo Park, Seul-gi Lee, Jong Bae Seo and Mina Lee
Pharmaceuticals 2024, 17(10), 1310; https://doi.org/10.3390/ph17101310 - 1 Oct 2024
Viewed by 677
Abstract
Background/Objectives: Moringa oleifera is a matrix plant with the high potential to cure several diseases with its medicinal and ethnopharmacological value and nutraceutical properties. In this study, we investigated the chemical and biological properties of this plant cultivated in our local region. [...] Read more.
Background/Objectives: Moringa oleifera is a matrix plant with the high potential to cure several diseases with its medicinal and ethnopharmacological value and nutraceutical properties. In this study, we investigated the chemical and biological properties of this plant cultivated in our local region. Methods: Leaves, roots, seeds, stem bark, and twigs of oleifera were extracted and evaluated bioactivities targeting intracellular lipid accumulation and adipocyte differentiation in 3T3-L1 preadipocytes, and UHPLC-ESI-Orbitrap-MS/MS-Based molecular networking guided isolation and dereplication of metabolites from these extracts. Results: Five extracts of different organs of M. oleifera significantly stimulated intracellular lipid accumulation and adipocyte differentiation in 3T3-L1 preadipocytes in a concentration-dependent manner. These extracts markedly increased the expression of genes related to adipogenesis and lipogenesis. Notably, these extracts promoted peroxisome proliferator-activated receptor γ (PPARγ) activity and the expression of its target genes, including phosphoenolpyruvate carboxykinase, fatty acid-binding protein 4, and perilipin-2. These adipogenic and lipogenic effects of Moringa extracts through the regulation of PPARγ activity suggests their potential efficacy in preventing or treating type 2 diabetes. Furthermore, chemical investigation revealed high contents of phytonutrients as rich sources of secondary metabolites including glycosides, flavones, fatty acids, phenolics, and other compounds. In addition, in silico studies on major components of these extracts revealed the bioavailability of major components through their binding affinity to respective proteins targeting adipocyte differentiation. Full article
(This article belongs to the Special Issue Exploring Natural Products as Modulators of Oxidative Stress in Health and Disease)
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Figure 1

Figure 1
<p>Stimulatory effects of Moringa extracts on adipocyte differentiation. The 3T3-L1 preadipocytes were cultured in a 0.1× differentiation induction medium for 6 days, either without (control) or with each Moringa extracts (100 μg/mL). (<b>A</b>) Cells were differentiated for 6 days were then stained with Nile Red to visualize lipid droplets and Hoechst 33342 to stain nuclei. Images were acquired by epifluorescence microscopy. Scale bar = 100 µm. (<b>B</b>,<b>C</b>) Quantification of Nile Red intensity and cell viability was performed using ImageJ software(version 1.54f). Nile Red fluorescence was normalized to the cell count determined by Hoechst 33342 staining. (<b>D</b>) mRNA expression levels of adipogenic genes were measured by qRT-PCR analysis. Data are shown as mean ± SEM (<span class="html-italic">n</span> = 4 per group). (<b>E</b>) The protein expression levels of PPARγ and adiponectin were analyzed using Western blotting. Results are shown as mean ± SEM (<span class="html-italic">n</span> = 2 per group). (<b>F</b>) mRNA expression levels of lipogenic genes were measured by qRT-PCR. Relative mRNA expression levels were normalized to 36B4 and are shown as mean ± SEM (<span class="html-italic">n</span> = 4 per group). All data are indicated as *, <span class="html-italic">p</span> &lt; 0.05; **, <span class="html-italic">p</span> &lt; 0.01; ***, <span class="html-italic">p</span> &lt; 0.001 versus control group.</p> Full article ">Figure 2
<p>Leaf extract of <span class="html-italic">M. oleifera</span> promotes adipocyte differentiation. The 3T3-L1 preadipocytes were cultured in a 0.1× differentiation induction medium for 6 days, either without (control) or with various concentrations of leaf extract (30, 100, and 300 μg/mL) of <span class="html-italic">M. oleifera</span>. (<b>A</b>) Following 6 days of differentiation, cells were stained with Nile Red and Hoechst 33342. Images were acquired by epifluorescence microscopy. Scale bar = 100 µm. (<b>B</b>,<b>C</b>) ImageJ software was used to quantify Nile Red staining intensity and cell viability. Data are shown as mean ± SEM (<span class="html-italic">n</span> = 4 per group). (<b>D</b>) mRNA expression levels of adipogenic genes were analyzed using qRT-PCR analysis. (<b>E</b>) Protein levels of PPARγ and Adiponectin were determined by Western blotting. Results are shown as mean ± SEM (<span class="html-italic">n</span> = 2 per group). (<b>F</b>) mRNA expression levels of lipogenic genes were measured by qRT-PCR analysis. Relative mRNA expression levels were normalized to 36B4 and are shown as mean ± SEM (<span class="html-italic">n</span> = 4 per group). All data are indicated as *, <span class="html-italic">p</span> &lt; 0.05; **, <span class="html-italic">p</span> &lt; 0.01; ***, <span class="html-italic">p</span> &lt; 0.001 versus control group.</p> Full article ">Figure 3
<p>Stem bark extract of <span class="html-italic">M. oleifera</span> induced adipocyte differentiation. The 3T3-L1 preadipocytes were cultured in a 0.1× differentiation induction medium for 6 days, either without (control) or with various concentrations of the stem bark extract (30, 100, and 300 μg/mL). (<b>A</b>) After 6 days, cells were stained with Nile Red and Hoechst33342. Images were acquired by epifluorescence microscopy. Scale bar = 100 µm. (<b>B</b>,<b>C</b>) Quantification of Nile Red intensity and cell viability was performed using ImageJ software. Data are shown as mean ± SEM (<span class="html-italic">n</span> = 4 per group). (<b>D</b>) mRNA expression levels of adipogenic genes were measured using qRT-PCR analysis. (<b>E</b>) Protein expression levels of PPARγ and adiponectin were assessed by Western blotting, with results shown as mean ± SEM (<span class="html-italic">n</span> = 2 per group). (<b>F</b>) mRNA expression levels of lipogenic genes were measured using qRT-PCR analysis. Relative mRNA expression levels were normalized to 36B4 and are shown as mean ± SEM (<span class="html-italic">n</span> = 4 per group). All data are presented as *, <span class="html-italic">p</span> &lt; 0.05; **, <span class="html-italic">p</span> &lt; 0.01; ***, <span class="html-italic">p</span> &lt; 0.001 versus control group.</p> Full article ">Figure 4
<p>Twig extract of <span class="html-italic">M. oleifera</span> stimulates the adipocyte differentiation of 3T3-L1 preadipocytes. Cells were cultured in a 0.1× differentiation induction medium for 6 days, either without (control) or with various concentrations of MRG twig extracts. (<b>A</b>) Cells differentiated for 6 days were stained with Nile Red and Hoechst33342. Images were acquired by epifluorescence microscopy. Scale bar = 100 µm. (<b>B</b>,<b>C</b>) The intensity of Nile Red staining and cell viability were quantified using ImageJ software. Results are shown as mean ± SEM (<span class="html-italic">n</span> = 4 per group). (<b>D</b>) mRNA expression levels of adipogenic genes were analyzed using qRT-PCR analysis. (<b>E</b>) Expression levels of PPARγ and adiponectin proteins were determined by Western blotting, with data shown as mean ± SEM (<span class="html-italic">n</span> = 2 per group). (<b>F</b>) mRNA expression levels of lipogenic genes were measured using qRT-PCR analysis. Relative mRNA levels were normalized to 36B4 and are presented as mean ± SEM (<span class="html-italic">n</span> = 4 per group). Statistical significance is indicated as *, <span class="html-italic">p</span> &lt; 0.05; **, <span class="html-italic">p</span> &lt; 0.01; ***, <span class="html-italic">p</span> &lt; 0.001 versus control group.</p> Full article ">Figure 5
<p>The leaf, stem bark, and twig extracts of <span class="html-italic">M. oleifera</span> increase PPARγ activity and the expression of PPARγ target genes. (<b>A</b>) h293a cells were transfected with DR-1-Luc, which contained three PPRE sequences upstream of the luciferase gene and indicated PPARγ and RXRα. After a day, indicated Moringa extracts of various doses (10, 30, and 100 μg/mL) or 10 μM of rosiglitazone were treated for a day. Measured luminescence levels were normalized with O.D values of the <span class="html-italic">β</span>-gal assay. N.S., not significant. (<b>B</b>) Differentiated adipocytes were seeded in a 12-well plate and treated with 100 μg/mL of indicated Moringa extracts or 10 μM rosiglitazone (positive control) or DMSO (negative group) for 2 days. Each RNA was used for qRT-PCR analysis. All data are presented as the mean ± SEM of two independent experiments (<span class="html-italic">n</span> = 4). *, <span class="html-italic">p</span> &lt; 0.05; **, <span class="html-italic">p</span> &lt; 0.01; ***, <span class="html-italic">p</span> &lt; 0.001 versus control group.</p> Full article ">Figure 6
<p>Chromatograms of five extracts of leaves (L), roots (R), seeds (S), stem bark (SB), and twigs (T) of <span class="html-italic">M</span>. <span class="html-italic">oleifera</span>.</p> Full article ">Figure 7
<p>Molecular docking of compounds <b>10</b> (cyan), <b>18</b> (blue), <b>28</b> (red), <b>37</b> (light orange), <b>41</b> (light blue), <b>43</b> (yellow), <b>46</b> (magenta), and co-crystallized ligand (2.4-thiazolidinedione, 5-[[4-[2-(methyl-2pyridinylamino)ethoxy]phenyl]methyl]-9cl, docked into PPARγ protein (PDB ID 4EMA).</p> Full article ">Figure 8
<p>Molecular docking of compounds <b>10</b> (cyan), <b>18</b> (blue), <b>28</b> (red), <b>37</b> (light orange), <b>41</b> (light blue), <b>43</b> (yellow), <b>46</b> (magenta), and the co-crystallized ligand ((2′-(5-ethyl-3,4-diphenyl-1H-pyrazol-1-yl)-3-biphenylyl)oxy)acetic acid, docked into FABP4 protein (PDB ID 2NNQ).</p> Full article ">Figure 9
<p>Molecular docking of compounds <b>10</b> (cyan), <b>18</b> (blue), <b>28</b> (red), <b>37</b> (light orange), <b>41</b> (light blue), <b>43</b> (yellow), <b>46</b> (magenta), docked into adiponectin protein (PDB ID: 6KS0).</p> Full article ">
18 pages, 9761 KiB  
Article
Phenylethanol Glycoside from Cistanche tubulosa Attenuates BSA-Induced Liver Fibrosis in Rats by Modulating the Gut Microbiota–Liver Axis
by Xinxin Qi, Hongguang Sun, Jincun Liu, Meili Cong, Xinxuan Zhang, Yuxin Yan, Zhaolin Xia, Tao Liu and Jun Zhao
Pharmaceuticals 2024, 17(9), 1149; https://doi.org/10.3390/ph17091149 - 30 Aug 2024
Viewed by 877
Abstract
This study aimed to investigate the effect of phenylethanol glycoside from Cistanche tubulosa (CPhGs) on the prevention of bovine serum albumin (BSA)-induced hepatic fibrosis in rats. Investigation of the mechanisms of the anti-hepatic fibrosis effect was focused on CPhGs’ influence on the “gut–liver” [...] Read more.
This study aimed to investigate the effect of phenylethanol glycoside from Cistanche tubulosa (CPhGs) on the prevention of bovine serum albumin (BSA)-induced hepatic fibrosis in rats. Investigation of the mechanisms of the anti-hepatic fibrosis effect was focused on CPhGs’ influence on the “gut–liver” regulation, including the gut microbiota, intestinal barrier, systemic lipopolysaccharide (LPS) concentration, and LPS-related signaling pathway. The results show that CPhGs restored the diversity of gut microbiota, increased the relative abundance of Bacteroidetes, and decreased the relative abundance of Firmicutes and Proteobacteria in the fibrotic rats. In addition, CPhGs promoted the enrichment of probiotics such as Blautia, Oscillospira, Ruminococcus, Odoribacter, Bacteroides, and Parabacteroides in intestines of these rats. Furthermore, CPhGs reduced histopathological injury in the intestine and restored the tight junctions of the intestine by increasing the expression of ZO-1, occludin, and E-cadherin. CPhGs efficiently reduced serum LPS and liver lipopolysaccharide-binding protein (LBP) levels and inhibited the LPS-TLR4/MyD88/NF-κB pathway, which is related to protein expression in the liver. Correlation analysis confirmed that these beneficial bacteria were negatively associated with pathological damage, while LPS and harmful bacteria were positively associated with liver injury. Our fecal microbiota transplantation (FMT) experiment confirmed that gut microbiota is an important part of disease progression and that CPhGs is useful for the prevention and treatment of hepatic fibrosis. Our data demonstrate that the anti-hepatic fibrosis mechanism of CPhGs was mediated by regulation of the “gut–liver” axis. These results can stimulate consideration for its use in clinical practices. Full article
(This article belongs to the Special Issue Exploring Natural Products as Modulators of Oxidative Stress in Health and Disease)
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Figure 1

Figure 1
<p>Effect of CPhGs on biochemical indicators and pathological changes in BSA-induced liver fibrosis rats. (<b>A</b>) Flowchart of the experimental protocol. (<b>B</b>) Changes in serum ALB, ALT, AST, TBIL, HA, PC-III, IV-C, and LN levels. (<b>C</b>) Pathological changes (arrows highlight the presence of portal fibrosis; for HE staining, the scale bar represents 100 or 200 µm; and for Sirius red staining, the scale bar represents 200 µm). Data are presented in violin charts, n = 6. * <span class="html-italic">p &lt;</span> 0.05, ** <span class="html-italic">p &lt;</span> 0.01, and *** <span class="html-italic">p &lt;</span> 0.001. ns: not significant.</p> Full article ">Figure 2
<p>Effects of CPhGs on protein expression of TLR-4/NF-κB in liver tissues. (<b>A</b>) changes of the LBP in liver tissue and LPS in serum. (<b>B</b>,<b>C</b>) expression and quantitative results of proteins related to the TLR-4/NF-κB signaling pathway. (<b>D</b>) changes of the TNF-α, IL-6, IL-1β expression in liver tissues. Data were presented as mean ± SD or in violin charts. n = 6, * <span class="html-italic">p &lt;</span> 0.05, and ** <span class="html-italic">p &lt;</span> 0.01, *** <span class="html-italic">p &lt;</span> 0.001. ns: not significant.</p> Full article ">Figure 3
<p>Effects of CPhGs on pathological observations of the intestinal tract. (<b>A</b>) effects of CPhGs on histomorphology in the ileum tissues (The yellow arrows point to fragmented intestinal villi; the green boxes circled are intestinal crypts, the scale bar represents 100 or 200 µm). (<b>B</b>) effects of CPhGs on histomorphology in the ileum and cecum tissues (The yellow boxes are secretory glands of the cecum, which were almost absent in the model group; the scale bar represents 100 or 200 µm). (<b>C</b>) the representative images of AB-PAS staining of intestinal tissues (The black arrows are immature goblet cells; the red arrows are goblet cells that are secreting; the scale bar represents 100 or 200 µm). (<b>D</b>) ultrastructural analysis in intestinal tissues by transmission electron microscopy (a: cell gap, b: intestinal villi, c: mitochondria, d: phagosome, at 30,000 µm magnification).</p> Full article ">Figure 4
<p>Effects of CPhGs intervention on intestinal barrier defects in rats with BSA-induced liver fibrosis. (<b>A</b>) Effects of CPhGs on IL-1β, IL-6, and TNF-α activities of gut tissues in BSA-induced liver fibrosis. (<b>B</b>) Effects of CPhGs on intestinal mucosa occludin, ZO-1, and E-cadherin protein expression in rats with BSA-induced liver fibrosis. Data are expressed as mean ± SD or in violin charts, n = 6, * <span class="html-italic">p &lt;</span> 0.05, ** <span class="html-italic">p &lt;</span> 0.01, and *** <span class="html-italic">p &lt;</span> 0.001.</p> Full article ">Figure 5
<p>Effects of CPhGs on gut microbiota dysbiosis in rats with BSA-induced liver fibrosis. (<b>A</b>) Chao1, Simpson, and Shannon indices analysis was performed to show α-diversity. (<b>B</b>) OTU Venn diagram. (<b>C</b>) Principal coordinate analysis (PCoA) was performed to show β-diversity. n = 6. * <span class="html-italic">p &lt;</span> 0.05, ** <span class="html-italic">p &lt;</span> 0.01. ns: not significant.</p> Full article ">Figure 6
<p>Effect of CPhGs on phylum levels of gut microbiota in rats with BSA-induced liver fibrosis. (<b>A</b>) Alterations of the intestinal flora comparison at the phylum, class, order, family, and genus levels. (<b>B</b>) Microbiota composition at the phylum level is shown. (<b>C</b>) Relative abundance of the dominant phylum of the intestinal flora compared in various groups (<span class="html-italic">Firmicutes, Bacteroidetes, Proteob</span>ac<span class="html-italic">teria</span>, and <span class="html-italic">Firmicutes</span>/<span class="html-italic">Bacteroidetes</span>). n = 6, * <span class="html-italic">p &lt;</span> 0.05, ** <span class="html-italic">p &lt;</span> 0.01.</p> Full article ">Figure 7
<p>Major species in the intestinal flora of the three groups of rats, identified using the LEfSe analysis. n = 6, LDA &gt; 4.</p> Full article ">Figure 8
<p>Modeling of gut microbiota in microbiota-depleted rats using the FMT assay. (<b>A</b>) Flow chart of FMT experiment. (<b>B</b>) Restoration of the intestinal flora at the phylum, class, order, family, and genus levels (n = 6). (<b>C</b>) Major species in the intestinal flora identified using LEfSe analysis (n = 6, LDA &gt; 3).</p> Full article ">Figure 9
<p>Effects of biochemical indices and pathological changes in FMT receptor rats. (<b>A</b>) Changes in serum ALT, AST, TBIL, and TP levels. (<b>B</b>) Changes in serum LPS, IL-1β, IL-6, and TNF-α. (<b>C</b>) Pathological changes (HE staining, 100×). Data are presented in violin charts, n = 6. * <span class="html-italic">p &lt;</span> 0.05, ** <span class="html-italic">p &lt;</span> 0.01, *** <span class="html-italic">p &lt;</span> 0.001. ns: not significant.</p> Full article ">
15 pages, 4959 KiB  
Article
Protective Effects of Lycium ruthenicum Murray against Acute Alcoholic Liver Disease in Mice via the Nrf2/HO-1/NF-κB Signaling Pathway
by Niantong Xia, Zimian Ding, Mingran Dong, Shuyang Li, Jia Liu, Hongwei Xue, Zhigang Wang, Juan Lu and Xi Chen
Pharmaceuticals 2024, 17(4), 497; https://doi.org/10.3390/ph17040497 - 13 Apr 2024
Cited by 2 | Viewed by 1155
Abstract
Acute alcoholic liver disease (ALD) resulting from short-term heavy alcohol consumption has become a global health concern. Moreover, anthocyanins have attracted much attention for their ability to prevent oxidation and inflammation. The present work evaluates the protective effects of Lycium ruthenicum Murray (LRM) [...] Read more.
Acute alcoholic liver disease (ALD) resulting from short-term heavy alcohol consumption has become a global health concern. Moreover, anthocyanins have attracted much attention for their ability to prevent oxidation and inflammation. The present work evaluates the protective effects of Lycium ruthenicum Murray (LRM) against ALD and explores the possible underlying mechanism involved. The total anthocyanin content in LRM was 43.64 ± 9.28 Pt g/100 g dry weight. Mice were orally administered 50, 125, or 375 mg LRM/kg body weight (BW) for 21 days. On days 18–21, mice were orally administered 15 mL of ethanol/kg BW. Markers of liver damage, oxidative stress, and inflammation were examined. Furthermore, the modulatory effect of LRM on Nrf2/HO-1/NF-κB pathway molecules was evaluated through quantitative reverse transcription polymerase chain reaction (RT‒qPCR) and immunohistochemistry analyses. The difference between the groups indicated that LRM improved liver histopathology and the liver index, decreased aspartate transaminase, alanine transaminase, malondialdehyde, reactive oxygen species, IL-6, TNF-α, and IL-1β expression, but elevated superoxide dismutase, catalase, and glutathione-s-transferase levels. Moreover, LRM upregulated Nrf2 and Ho-1 but downregulated Nf-κb and Tnf-α genes at the transcript level. In summary, LRM alleviated ethanol-induced ALD in mice by reducing oxidative damage and associated inflammatory responses. LRM protects against ALD by reducing damage factors and enhancing defense factors, especially via the Nrf2/HO-1/NF-κB pathway. Thus, LRM has application potential in ALD prophylaxis and treatment. Full article
(This article belongs to the Special Issue Exploring Natural Products as Modulators of Oxidative Stress in Health and Disease)
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Graphical abstract

Graphical abstract
Full article ">Figure 1
<p>Histopathological sections from each group. (means ± SD, <span class="html-italic">n</span>= 6). (<b>a</b>) NC. Scale bar: 100 μm; (<b>b</b>) M. Scale bar: 100 μm; (<b>c</b>) S. Scale bar: 100 μm; (<b>d</b>) LL. Scale bar: 100 μm; (<b>e</b>) LM. Scale bar: 100 μm; (<b>f</b>) LH. Scale bar: 100 μm; (<b>g</b>) liver organ indices. ## <span class="html-italic">p</span> &lt; 0.01 vs. the normal control group; * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01 vs. the model group.</p> Full article ">Figure 2
<p>Alterations in the serum ALT, AST, TC, TG, LDL-c, and LDH contents among C57BL/6J mice after administration of 15 mL alcohol/kg body weight. Red star Erguotou liquor at 56° (means ± SD, <span class="html-italic">n</span> = 6) (<b>a</b>) ALT; (<b>b</b>) AST; (<b>c</b>) TC; (<b>d</b>) TG; (<b>e</b>) LDL-C; (<b>f</b>) LDH. ## <span class="html-italic">p</span> &lt; 0.01 vs. the normal control group; * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01 vs. the model group.</p> Full article ">Figure 3
<p>Changes in serum ROS concentration in C57BL/6J mice after administering 15 mL of ethanol/kg body weight. (means ± SD, <span class="html-italic">n</span> = 6). ## <span class="html-italic">p</span> &lt; 0.01 vs. the normal control group; * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01 vs. the model group.</p> Full article ">Figure 4
<p>Changes in CAT, GST, MDA, and SOD contents in liver tissue from C57BL/6J mice after administering 15 mL of ethanol/kg body weight. (means ± SD, <span class="html-italic">n</span> = 6). (<b>a</b>) CAT content; (<b>b</b>) GST content; (<b>c</b>) MDA content; (<b>d</b>) SOD content. ## <span class="html-italic">p</span> &lt; 0.01 vs. the normal control group; * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01 vs. the model group.</p> Full article ">Figure 5
<p>Changes in IL-6, TNF-α, and IL-1β levels in liver tissue from C57BL/6J mice after administering 15 mL of ethanol/kg body weight. (means ± SD, <span class="html-italic">n</span> = 6). (<b>a</b>) IL-6; (<b>b</b>) TNF-α; (<b>c</b>) IL-1β levels. ## <span class="html-italic">p</span> &lt; 0.01 vs. the normal control group; * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01 vs. the model group.</p> Full article ">Figure 6
<p>mRNA expression in the normal control group. (means ± SD, <span class="html-italic">n</span> = 6). (<b>a</b>) <span class="html-italic">Nrf2</span>, (<b>b</b>) <span class="html-italic">Ho-1</span>, (<b>c</b>) <span class="html-italic">Nf-κb</span>, (<b>d</b>) <span class="html-italic">Tnf-α</span>. # <span class="html-italic">p</span> &lt; 0.05, ## <span class="html-italic">p</span> &lt; 0.01 vs. the normal control group; * <span class="html-italic">p</span> &lt; 0.05 vs. the model group.</p> Full article ">Figure 7
<p>Immunohistochemical staining analysis of Nrf2, HO-1, and NF-κB in each group. (means ± SD, <span class="html-italic">n</span> = 6). (<b>b</b>) Nrf2, (<b>c</b>) HO-1, (<b>d</b>) NF-κB. ## <span class="html-italic">p</span> &lt; 0.01 vs. the normal control group; * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01 vs. the model group.</p> Full article ">
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