Arginyl-fructosyl-glucose, a major Maillard reaction product of red ginseng mitigates cisplatin-evoked intestinal toxicity<i>in vivo</i>and<i>in vitro</i>

Liu, Wei; Zhang, Hao; Hou, Yun-yi; Hu, Rui-Yi; Zhang, Junjie; Chen, Xuan; Wang, Shuang; Hu, Jun‐Nan; Wang, Zi; Li, Wei

doi:10.1039/d2fo00776b

Cited by 10 publications

(3 citation statements)

References 52 publications

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“…After deparaffinage, liver sections were subject to rehydration, immersion in 0.3%H2O2 for 5min to eliminate endogenous peroxidase, and 15-min incubation with citrate buffer (pH 6.0) to achieve antigen recovery by boiling. Later, 0.1%Triton X-100 was added to permeate sections, followed by treated with 10% goat serum for non-specific antigen blocking [18].…”

Section: Immunofluorescence (If)mentioning

confidence: 99%

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Alleviation of D-gal-induced senile liver injury by Rg3, a signature component of red ginseng

Ding

et al. 2023

Aging

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To investigate the mechanism by which ginsenoside Rg3 regulates oxidative stress (OS) and inflammation through NF/KB pathway to delay mouse liver injury. This work randomized Balbc mice as four groups: Normal, D-gal, Rg3-L, Rg3-H. Paraffin-embedded liver tissue sections were prepared, later, BAX/BCL-2 protein expression was observed by HE, Sirius red, TUNEL and immunofluorescence to detect apoptotic injury and α-SMA/TGF-β protein expression to detect fibrosis, and liver inflammation-related protein NF-KB was detected. HE and TUNEL staining showed that Rg3 reduced necrotic cells and fibrosis in liver-injured mice, Rg3 increased anti-inflammatory cytokine IL-18 and reduced TNF-α, IL-1β and IL-6 expression. Conclusion: Ginsenoside Rg3 can effectively antagonize D-gal's role in mouse liver injury, and its mechanism may be associated with regulating inflammatory pathway by Rg.

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Section: Immunofluorescence (If)mentioning

confidence: 99%

“…The fluorescence microscope was employed to capture images. Signal intensities were analyzed using ImageJ software and determined through calculating mean unit intensity to control [18].…”

Section: Immunofluorescence (If)mentioning

confidence: 99%

Alleviation of D-gal-induced senile liver injury by Rg3, a signature component of red ginseng

Ding

et al. 2023

Aging

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“…The cells were collected after trypsin digestion, and the levels of oxidative indicators (MDA) and antioxidant indicators (SOD, GSH, and CAT) were analyzed with enzyme-linked immunosorbent assay (ELISA) kits. The absorbance values at OD 450 were measured, and the MDA levels together with the SOD, GSH, and CAT activities were calculated [18]. The MDA (Cat# A003-1-2), SOD (Cat# A001-1-2), GSH (Cat# A006-2-1), and CAT (Cat# A007-1-1) assay kits were purchased from the Nanjing Jiancheng Bioengineering Institute (Nanjing, China).…”

Section: Oxidative and Antioxidant Function Assessmentmentioning

confidence: 99%

Baicalin Exhibits a Protective Effect against Cisplatin-Induced Cytotoxic Damage in Canine Renal Tubular Epithelial Cells

Wang,

Li,

Yan

et al. 2023

Metabolites

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Renal failure is a common chronic disease in dogs that substantially affects both their quality of life and longevity. The objective of this study was to assess the protective mechanisms of baicalin in cisplatin-induced Madin–Darby canine kidney (MDCK) epithelial cells’ apoptosis model and explore the impacts of baicalin at varying doses on various indexes, such as cisplatin-induced MDCK cell apoptosis, oxidation and antioxidation, and inflammatory factors. (Methods) MDCK cells in the logarithmic growth phase were randomly divided into a control group, a model group (20 μmol/L cisplatin), and a baicalin-protection group (20 μmol/L cisplatin + 50, 25 μmol/L baicalin) and received the corresponding treatments for 24 h. The effects of cisplatin on MDCK cell apoptosis, oxidation and antioxidation, inflammatory factors, and other indicators were studied, and the relieving effect of baicalin on cisplatin-induced MDCK cell damage was explored. Calcein/PI staining and Annexin V-FITC/PI staining showed that cisplatin induced the apoptosis of MDCK cells, while baicalin effectively reduced the damage caused by cisplatin. The ELISA results demonstrated a significant elevation in the nitric oxide (NO) and malondialdehyde (MDA) levels within the MDCK cells following treatment with cisplatin (p < 0.01). In addition, superoxide dismutase (SOD), glutathione peroxidase (GSH), and catalase (CAT) activities remarkably declined (p < 0.01), while tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) expression within the MDCK cells were apparently elevated (p < 0.01). However, baicalin treatment resulted in opposite changes in these factors. The findings suggested that baicalin exhibits potential in mitigating cisplatin-induced oxidative stress and inflammation in MDCK cells. As revealed with the Western blot results, cisplatin promoted P62, P53, and BAX protein levels, increased mTOR phosphorylation, inhibited AMPK phosphorylation, and reduced Beclin1 and BCL-2 protein levels. However, a contrasting trend was observed following baicalin treatment. Cisplatin can inhibit the activity of MDCK cells, lead to abnormalities in oxidation and antioxidation functions and cell inflammatory factors, and accelerate cell apoptosis. Moreover, baicalin can significantly alleviate the damage of cisplatin to MDCK cells.

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Xiao‐Ban‐Xia Decoction Alleviates Chemotherapy‐Induced Nausea and Vomiting by Inhibiting Ferroptosis via Activation of The Nrf2/SLC7A11/GPX4 Pathway

Liang,

Ren,

Wang

et al. 2024

Advanced Biology

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Chemotherapy‐induced nausea and vomiting (CINV) represents the common gastrointestinal side effect for cancer patients. Xiao‐Ban‐Xia decoction (XBXD), a classical anti‐emetic traditional Chinese medicine formula, is frequently used for the clinical treatment of CINV. This study used a cisplatin‐induced rat pica model to explore whether the anti‐emetic mechanism of XBXD in treating CINV is related to ferroptosis. The inflammatory damage of the gastrointestinal tract is evaluated by HE staining and ELISA. The degree of ferroptosis are validated by the iron deposition, the levels of ROS, MDA, and GSH, and the ultrastructure of mitochondria in the gastric antrum and ileum. The potential ferroptosis‐related targets of XBXD against CINV are screened by network pharmacology and further assessed by Western blot. XBXD significantly decreased the kaolin consumption in rats, and improved the inflammatory pathological damage, with decreased levels of HMGB1, IL‐1β, and TNF‐α. Furthermore, XBXD significantly suppressed ferroptosis, as indicated by the improvement of iron deposition, mitochondrial abnormalities, and oxidative stress. The network pharmacology and Western blot results indicated that XBXD activated the Nrf2/SLC7A11/GPX4 signaling pathway. This study proved that XBXD activates the Nrf2/SLC7A11/GPX4 signaling pathway, thereby inhibiting ferroptosis, which represents a critical anti‐emetic mechanism of XBXD in combatting CINV.

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Arginyl-fructosyl-glucose, a major Maillard reaction product of red ginseng mitigates cisplatin-evoked intestinal toxicityin vivoandin vitro

Abstract: Cisplatin-evoked profound gastrointestinal symptomatology is one of the most common side effects of chemotherapy drugs, further causing gastrointestinal cell damage, diarrhea and vomiting. Panax ginseng C. A. Meyer, a widely...

Cited by 10 publications

References 52 publications

Alleviation of D-gal-induced senile liver injury by Rg3, a signature component of red ginseng

Alleviation of D-gal-induced senile liver injury by Rg3, a signature component of red ginseng

Baicalin Exhibits a Protective Effect against Cisplatin-Induced Cytotoxic Damage in Canine Renal Tubular Epithelial Cells

Xiao‐Ban‐Xia Decoction Alleviates Chemotherapy‐Induced Nausea and Vomiting by Inhibiting Ferroptosis via Activation of The Nrf2/SLC7A11/GPX4 Pathway

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