Daucosterol Alleviates Alcohol−Induced Hepatic Injury and Inflammation through P38/NF−κB/NLRP3 Inflammasome Pathway

Zhang, Feng; Wang, Mengyao; Zha, Yang; Zhou, Jie; Han, Jihong; Zhang, Shuang

doi:10.3390/nu15010223

Cited by 14 publications

(8 citation statements)

References 60 publications

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“…ERK and JNK were unchanged after chronic stress or CGA treatment. p38MAPK is an important member of MAPK, which is not only involved in the cell cycle, development, differentiation, cell death, senescence, and tumorigenesis, but also acts as a specific serine/threonine kinase to regulate inflammation. , A large number of studies have shown that p38 could activate the NF-κB signaling pathway, thereby causing inflammation in some diseases such as IBD, alcohol-induced hepatic injury, lung inflammation, and Parkinson’s. − After SB203580 intervention, the phosphorylation level of p65 was significantly reduced, and the transcription and translation levels of TNF were significantly reduced. The intestinal damage was also significantly reduced.…”

Section: Discussionmentioning

confidence: 99%

Chlorogenic Acid Alleviates Chronic Stress-Induced Intestinal Damage by Inhibiting the P38MAPK/NF-κB Pathway

Zhao,

Wang,

Yang

et al. 2023

J. Agric. Food Chem.

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Chronic stress can cause intestinal barrier damage. MAPK and NF-κB are closely related to it. Chlorogenic acid (CGA), a dietary polyphenol, has been shown to have intestinal protective effects, but whether by regulating MAPK and NF-κB is not known. Therefore, in this experiment, 24 Wistar rats were randomly divided into 4 groups (C group, CS group, CS + SB203580, and CS + CGA group). Rats in the CS group were restrained stress for 6 h per day for 21 days. Rats in the CS + SB203580 group were given SB203582 (0.5 mg/kg, intraperitoneal injection) 1 h before restraint stress every other day. Rats in the CS + CGA group were given CGA (100 mg/kg, gavage) 1 h before restraint stress. In chronic stress, intestinal barrier damage was evident, while being restored after CGA treatment. After chronic stress, the levels of p-P38 were increased (P < 0.01), while the levels of p-JNK and p-ERK were not changed. The levels of p-p38 were elevated after CGA treatment (P < 0.01). These results suggested that p38MAPK played an important role in chronic stress-induced intestinal injury, and CGA could inhibit p38MAPK activity. Therefore, we chose SB203582 (P38MAPK inhibitor) to elucidate the role of p38. After chronic stress, intestinal tight junction key proteins Occludin, ZO-1, and Claudin3 protein and gene expression were reduced (P < 0.01), while being elevated after CGA or SB203582 intervention (P < 0.05). After CGA treatment, the levels of p-IκB, p-p65, p-p38, and TNF-α were reduced (P < 0.01). SB203582 intervention reduced p-p65 and TNF-α levels significantly (P < 0.01). These results suggested that CGA could inhibit the NF-κB pathway by suppressing p38MAPK, thereby alleviating chronic stress-induced intestinal damage.

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Section: Discussionmentioning

confidence: 99%

Chlorogenic Acid Alleviates Chronic Stress-Induced Intestinal Damage by Inhibiting the P38MAPK/NF-κB Pathway

Zhao,

Wang,

Yang

et al. 2023

J. Agric. Food Chem.

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“…Li et al [ 36 ] used MG132 to inhibit the NF- κ B pathway and reduce the extent of liver injury. Some natural antioxidants can also protect against IRI through their own antioxidant effects and inhibition of the NF- κ B pathway [ 37 ]. Ischemic preconditioning can also reduce the activation of the NF- κ B pathway during the subsequent IR process to some extent, resulting in a protective effect on organs.…”

Section: Discussionmentioning

confidence: 99%

Aldehyde Dehydrogenase 2 Protects the Kidney from Ischemia–Reperfusion Injury by Suppressing the IκBα/NF-κB/IL-17C Pathway

Chen

Xiong

Luo

et al. 2023

Oxidative Medicine and Cellular Longevity

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Objective. Ischemia–reperfusion injury (IRI) is an important cause of delayed functional recovery after transplantation. This study is aimed at investigating the molecular mechanism of ALDH2 in a kidney ischemia–reperfusion model based on RNA-seq. Methods. We performed kidney ischemia–reperfusion in ALDH2-/- and WT mice and evaluated kidney function and morphology using SCr, HE staining, TUNEL staining, and TEM. We used RNA-seq to compare mRNA expression in ALDH2-/- and WT mice after IR, and then, we verified the related molecular pathways by PCR and western blotting. In addition, activators and inhibitors of ALDH2 were used to alter the activity of ALDH2. Finally, we established a model of hypoxia and reoxygenation in HK-2 cells and clarified the role of ALDH2 in IR by interfering with ALDH2 and using an NF-κB inhibitor. Results. After kidney ischemia–reperfusion, the SCr value increased significantly, kidney tubular epithelial cells were damaged, and the apoptosis rate increased. In the microstructure, mitochondria were swollen and deformed, and ALDH2 deficiency aggravated these changes. The NF-κB pathway and IL-17 pathway were significantly enriched in ALDH2-/- mice compared with WT mice according to KEGG enrichment analysis of the RNA-seq data. The PCR results showed that the mRNA expression levels of IκBα and IL-17B, C, D, E, and F were significantly higher than those in the WT-IR group. Western blot verification results showed that ALHD2 knockdown resulted in increased phosphorylation of IκBα, increased phosphorylation of NF-κB, and increased expression of IL-17C. When we used ALDH2 agonists, the number of lesions and the expression levels of the corresponding proteins were reduced. Knockdown of ALDH2 in HK-2 cells resulted in a higher proportion of apoptotic cells after hypoxia and reoxygenation, but inhibiting the phosphorylation of NF-κB prevented the increase in apoptosis and reduced the protein expression level of IL-17C. Conclusion. ALDH2 deficiency can lead to the aggravation of kidney ischemia–reperfusion injury. RNA-seq analysis and validation by PCR and western blotting revealed that this effect may be due to the promotion of IκBα/NF-κB p65 phosphorylation during ischemia–reperfusion caused by ALDH2 deficiency, which then leads to an increase in inflammatory factors, including IL-17C. Thus, cell death is promoted, and kidney IRI is eventually aggravated. We link ALDH2 deficiency with inflammation, revealing a new idea for ALDH2-related research.

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“…Studies have shown that daucosterol intervention can effectively reduce liver injury, reduce liver index, TNF-α and IL-1β/6 expression levels, and attenuate liver injury in mouse models of liver failure by regulating the IL-6/STAT3 signaling pathway [ 94 ]. Daucosterol also plays a key role in the prevention of liver cancer by improving alcohol-induced liver injury through the p38/NF-κB/NLRP3 signaling pathway, as well as preventing liver oxidative stress and lipid accumulation [ 95 ]. Liver fibrosis is an important factor leading to cirrhosis and subsequently liver cancer, and the activation of hepatic stellate cells is the main cause of liver fibrosis.…”

Section: Prevention Of Precancerous Lesionsmentioning

confidence: 99%

Research progress of Paris polyphylla in the treatment of digestive tract cancers

Wang,

Ni,

Wang

et al. 2024

Discov Onc

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Cancer has become one of the most important causes of human death. In particular, the 5 year survival rate of patients with digestive tract cancer is low. Although chemotherapy drugs have a certain efficacy, they are highly toxic and prone to chemotherapy resistance. With the advancement of antitumor research, many natural drugs have gradually entered basic clinical research. They have low toxicity, few adverse reactions, and play an important synergistic role in the combined targeted therapy of radiotherapy and chemotherapy. A large number of studies have shown that the active components of Paris polyphylla (PPA), a common natural medicinal plant, can play an antitumor role in a variety of digestive tract cancers. In this paper, the main components of PPA such as polyphyllin, C21 steroids, sterols, and flavonoids, amongst others, are introduced, and the mechanisms of action and research progress of PPA and its active components in the treatment of various digestive tract cancers are reviewed and summarized. The main components of PPA have been thoroughly explored to provide more detailed references and innovative ideas for the further development and utilization of similar natural antitumor drugs.

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Daucosterol Alleviates Alcohol−Induced Hepatic Injury and Inflammation through P38/NF−κB/NLRP3 Inflammasome Pathway

Cited by 14 publications

References 60 publications

Chlorogenic Acid Alleviates Chronic Stress-Induced Intestinal Damage by Inhibiting the P38MAPK/NF-κB Pathway

Chlorogenic Acid Alleviates Chronic Stress-Induced Intestinal Damage by Inhibiting the P38MAPK/NF-κB Pathway

Aldehyde Dehydrogenase 2 Protects the Kidney from Ischemia–Reperfusion Injury by Suppressing the IκBα/NF-κB/IL-17C Pathway

Research progress of Paris polyphylla in the treatment of digestive tract cancers

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