Autophagy: A potential target for natural products in the treatment of ulcerative colitis

Zhang, Wei; Zou, Menglong; Fu, Jia; Xu, Yin; Zhu, Ying

doi:10.1016/j.biopha.2024.116891

Cited by 5 publications

References 245 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Investigation of oral toxicity of WS₂ nanosheets to mouse intestine: Pathological injury, trace element balance, lipid profile changes, and autophagy

Zha,

Luo,

Wei

et al. 2024

J of Applied Toxicology

View full text Add to dashboard Cite

The success of graphene oxides has gained extensive research interests in developing novel 2D nanomaterials (NMs). WS2 nanosheets (NSs) are novel transition metal‐based 2D NMs, but their toxicity is unclear. In this study, we investigated the oral toxicity of WS2 NSs to mouse intestines. Male mice were administrated with vehicles, 1, 10, or 100 mg/kg NSs via intragastric route, once a day, for 5 days. The results indicate that the NSs did not induce pathological or ultrastructural changes in intestines. There were minimal changes of trace elements that the exposure did not induce W accumulation, and only Co levels were dose‐dependently increased. Lipid droplets were observed in all groups of mice, but lipidomics data indicate that WS2 NSs only significantly decreased four lipid species, all belonging to phosphatidylcholine (PC). The levels of proteins regulating autophagic lipolysis, namely, LC3, lysosomal associated membrane protein 2 (LAMP2) and perilipin 2 (PLIN2), were increased, but it was only statistically significantly different for LC3. The results of this study suggest that repeated intragastric exposure to WS2 NSs only induced minimal influences on pathological injury, trace element balance, autophagy, and lipid profiles in mouse intestines, indicating relatively high biocompatibility of WS2 NSs to mouse intestine via oral route.

show abstract

Investigation of oral toxicity of WS₂ nanosheets to mouse intestine: Pathological injury, trace element balance, lipid profile changes, and autophagy

Zha,

Luo,

Wei

et al. 2024

J of Applied Toxicology

View full text Add to dashboard Cite

show abstract

Epimedium polysaccharides ameliorate ulcerative colitis by inhibiting oxidative stress and regulating autophagy

Zhao,

Jiang,

Zhang

et al. 2024

J Sci Food Agric

View full text Add to dashboard Cite

BACKGROUNDEpimedium polysaccharide (EPS) is a bioactive compound derived from the traditional Chinese herb Epimedium brevicornum. The objective of this study was to investigate the protective effects of EPS on ulcerative colitis (UC) and to elucidate the underlying mechanisms involved.RESULTSThe findings showed that EPS treatment mitigated UC symptoms, including weight loss, anal bleeding, elevated disease activity index (DAI), and colon shortening. Hematoxylin and eosin (H&E) and Alcian blue–periodic acid–Schiff (AB‐PAS) staining demonstrated that EPS alleviated histopathological damage and improved the integrity of the colonic mucosa. Mechanistically, EPS was found to substantially decrease inflammation by inhibiting the Toll‐like receptor 4/nuclear factor‐κB (TLR4/NF‐κB) signaling pathway and to alleviate oxidative stress through modulation of the Kelch‐like ECH‐associated protein 1/nuclear factor erythroid‐derived 2‐like 2 (Keap1/Nrf2) pathway. Notably, EPS failed to exert protective effects against dextran sulfate sodium (DSS)‐induced UC in Nrf2‐knockout (Nrf2−/−) mice. Additionally, Western blotting and immunohistochemical analysis demonstrated that EPS facilitated autophagy via the adenosine monophosphate‐dependent protein kinase/mammalian target of rapamycin (AMPK/mTOR) pathway. In vitro experiments revealed that EPS effectively suppressed lipopolysaccharide (LPS)‐mediated cellular damage and oxidative stress by regulating Keap1/Nrf2 pathway. Transcriptomic analysis of LPS‐treated Caco‐2 cells following EPS treatment revealed a significant up‐regulation of Nrf2 expression.CONCLUSIONIn conclusion, the findings of this study suggest that EPS exerts protective effects against DSS‐induced UC through the inhibition of the TLR4/NF‐κB signaling pathway, regulation of the Keap1/Nrf2 pathway, and promotion of autophagy via the AMPK/mTOR pathway. Consequently, EPS may represent a potential therapeutic target for the treatment of UC. © 2024 Society of Chemical Industry.

show abstract

The mechanisms behind heatstroke-induced intestinal damage

Sun,

Li,

Zou

et al. 2024

Cell Death Discov.

View full text Add to dashboard Cite

With the frequent occurrence of heatwaves, heatstroke (HS) is expected to become one of the main causes of global death. Being a multi-organized disease, HS can result in circulatory disturbance and systemic inflammatory response, with the gastrointestinal tract being one of the primary organs affected. Intestinal damage plays an initiating and promoting role in HS. Multiple pathways result in damage to the integrity of the intestinal epithelial barrier due to heat stress and hypoxia brought on by blood distribution. This usually leads to intestinal leakage as well as the infiltration and metastasis of toxins and pathogenic bacteria in the intestinal cavity, which will eventually cause inflammation in the whole body. A large number of studies have shown that intestinal damage after HS involves the body’s stress response, disruption of oxidative balance, disorder of tight junction proteins, massive cell death, and microbial imbalance. Based on these damage mechanisms, protecting the intestinal barrier and regulating the body’s inflammatory and immune responses are effective treatment strategies. To better understand the pathophysiology of this complex process, this review aims to outline the potential processes and possible therapeutic strategies for intestinal damage after HS in recent years.

show abstract

Autophagy: A potential target for natural products in the treatment of ulcerative colitis

Cited by 5 publications

References 245 publications

Investigation of oral toxicity of WS₂ nanosheets to mouse intestine: Pathological injury, trace element balance, lipid profile changes, and autophagy

Investigation of oral toxicity of WS₂ nanosheets to mouse intestine: Pathological injury, trace element balance, lipid profile changes, and autophagy

Epimedium polysaccharides ameliorate ulcerative colitis by inhibiting oxidative stress and regulating autophagy

The mechanisms behind heatstroke-induced intestinal damage

Contact Info

Product

Resources

About

Autophagy: A potential target for natural products in the treatment of ulcerative colitis

Cited by 5 publications

References 245 publications

Investigation of oral toxicity of WS2 nanosheets to mouse intestine: Pathological injury, trace element balance, lipid profile changes, and autophagy

Investigation of oral toxicity of WS2 nanosheets to mouse intestine: Pathological injury, trace element balance, lipid profile changes, and autophagy

Epimedium polysaccharides ameliorate ulcerative colitis by inhibiting oxidative stress and regulating autophagy

The mechanisms behind heatstroke-induced intestinal damage

Contact Info

Product

Resources

About

Investigation of oral toxicity of WS₂ nanosheets to mouse intestine: Pathological injury, trace element balance, lipid profile changes, and autophagy

Investigation of oral toxicity of WS₂ nanosheets to mouse intestine: Pathological injury, trace element balance, lipid profile changes, and autophagy