Eriodictyol inhibits high glucose‐induced extracellular matrix accumulation, oxidative stress, and inflammation in human glomerular mesangial cells

Bai, Jingwei; Wang, Yi; Zhu, Xiaodong; Shi, Jun

doi:10.1002/ptr.6463

Cited by 36 publications

(17 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition to autophagy, there are a large number of inflammatory cytokines release and neuronal apoptosis, and other pathological processes in cerebral ischemia-reperfusion injury. It has been (Bai et al, 2019 ) reported that eriodictyol could suppress the activation of Akt/NF-κB to inhibit inflammation and oxidative stress in HG-induced human glomerular mesangial cells. Eriodictyol can improve LPS-induced inflammatory response and oxidative stress by inhibiting MAPKs and NF-κB pathways and balancing Nrf2/KeAP1 antioxidant defense pathway in BV-2 microglial cells and mouse brain (He et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Eriodictyol Attenuates MCAO-Induced Brain Injury and Neurological Deficits via Reversing the Autophagy Dysfunction

Wang

Ma²,

Wang³

et al. 2021

Front. Syst. Neurosci.

View full text Add to dashboard Cite

The present study was designed to investigate the protective effect of eriodictyol on MCAO-induced brain injury and its regulation of neural function and to explore the mechanism of its regulation of autophagy in rats. Brain injury was induced by middle cerebral artery occlusion (MCAO) in adult rats and pretreated with eriodictyol (low dose: 20 mg/kg; medium dose: 40 mg/kg; high dose: 80 mg/kg) or saline. Rats in the treatment group had a smaller volume of infarction and improved neurological outcome and reduced the latency to the platform, increased the time spent in the correct quadrant compared to MCAO rats pretreated with saline. ELISA kits results confirmed that eriodictyol reduced the inflammatory response induced by MCAO. The results of apoptosis and proliferation by Nissl staining and immunofluorescence detection indicated that eriodictyol could inhibit apoptosis and promote the proliferation in MCAO rats. The expressions of LC3, ATG5, p62, and Beclin1 were used to evaluate the autophagy, as well as the reversal of the autophagy activator (rapamycin) on the neuroprotective effect of eriodictyol, which suggested that the protective effect of eriodictyol on brain injury may be related to the inhibition of autophagy. In summary, we, therefore, suggested that eriodictyol could reduce the inflammation response of brain injury and inhibit neuroapoptosis, directly affecting autophagy to alleviate brain injury. It will provide theoretical support for eriodictyol in the treatment of ischemic stroke.

show abstract

Section: Discussionmentioning

confidence: 99%

Eriodictyol Attenuates MCAO-Induced Brain Injury and Neurological Deficits via Reversing the Autophagy Dysfunction

Wang

Ma²,

Wang³

et al. 2021

Front. Syst. Neurosci.

View full text Add to dashboard Cite

show abstract

“…NOX is critical for the production of reactive oxygen species (ROS), leading to oxidative stress that contributes to DN development [ 50 , 51 ] [ 52 , 53 ]. Furthermore, high glucose can induce NOX2 expression, leading to oxidative stress in renal tubular epithelial and glomerular mesangial cells [ 74 , 75 ]. TXNIP acts as an endogenous TRX inhibitor that reduces TRX protein activity and expression [ 76 ].…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic Analysis Reveals the Protection of Astragaloside IV against Diabetic Nephropathy by Modulating Inflammation

Zhang

Tao

Chen

et al. 2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Background. Diabetic nephropathy (DN) is one of the leading causes of end-stage kidney disease. Recently, there is no specific drug available to block the kidney damage. Astragaloside IV (AS-IV) is a major active component of Astragalus membranaceus (Fisch) Bge and has been demonstrated to benefit the kidney functions. This study explores the potential pharmacological action of AS-IV in DN of rats. Methods. Male Sprague-Dawley rats were fed with high-fat diet and injected with streptozotocin to induce diabetes. The diabetic rats were randomized and treated with vehicle or AS-IV (80 mg/kg) daily by gavage for 12 weeks as the DN or AS-IV group, respectively. The normal control rats were fed with normal chow and injected with vehicles (n=8 per group). These rats were monitored for diabetes- and kidney function-related measures. The expression profiles of gene mRNA transcripts in the kidney tissues were analyzed by RNA-seq and quantitative RT-PCR. The levels of advanced glycation end products (AGEs), IL-1β, and IL-18 in the serum samples and kidney tissues were quantified by ELISA. The levels of collagen IV (COL-4) and fibronectin (FN) expression in kidney tissues were examined by immunohistochemistry and Western blot. Results. In comparison with the DN group, AS-IV treatment significantly reduced blood glucose levels, food and water consumption, 24 h urine, renal index values, 24 h urine total proteins, blood urea nitrogen (BUN) levels, and creatinine clearance rates (CCR), accompanied by minimizing the DN-induced early kidney damages, fibrosis, and microstructural changes. Furthermore, AS-IV treatment significantly modulated the DN-altered gene transcription profiles in the kidney of rats, particularly for inflammation-related genes, including the nucleotide-binding oligomerization domain-like receptor signaling, which was validated by quantitative RT-PCR. AS-IV treatment significantly decreased the levels of serum and kidney AGEs, IL-1β, and IL-18 expression and fibrosis indexes in the kidney of rats. Conclusion. AS-IV treatment ameliorated the severity of DN by inhibiting inflammation-related gene expression in the kidney of rats.

show abstract

“…As we know that reactive oxygen species (ROS) and inflammation are tightly linked [30,31], we want to know whether ROS was involved in inflammation in SW480 and HCT116 cells. The results demonstrated that LPS could promote ROS accumulation (Fig.…”

Section: Hmgb1 Regulates Inflammation Via Ros-mediatedmentioning

confidence: 99%

HMGB1 mediates lipopolysaccharide-induced inflammation via interacting with GPX4 in colon cancer cells

Yang

Jiang

et al. 2020

Cancer Cell Int

View full text Add to dashboard Cite

Background Inflammation is one of a main reason for colon cancer progression and poor prognosis. The high-mobility group box-1 (HMGB1) and glutathione peroxidase 4 (GPX4) are responsible for inflammation, but the relationship between HMGB1 and GPX4 remains unknown about inflammation in colon cancer. Methods RT-qPCR was carried out to investigate the expression of IL1β, IL6 and TNFα in colon cancer cells stimulated with LPS or siHMGB1. To observe the relationship between HMGB1, GPX4 and inflammation or ROS, Western blot assays were adopted. Pull-down, CoIP and immunohistochemistry assays were performed to further investigate the molecular mechanisms of HMGB1 and GPX4 in colon cancer. Results We report that HMGB1 mediates lipopolysaccharide (LPS)-induced inflammation in colon cancer cells. Mechanistically, acetylated HMGB1 interacts with GPX4, negatively regulating GPX4 activity. Furthermore, by utilizing siHMGB1 and its inhibitor, our discoveries demonstrate that HMGB1 knockdown can inhibit inflammation and reactive oxygen species (ROS) accumulation via NF-kB. Conclusion Collectively, our findings first demonstrate that acetylated HMGB1 can interact with GPX4, leading to inflammation, and providing therapeutic strategies targeting HMGB1 and GPX4 for colon cancer.

show abstract

Eriodictyol inhibits high glucose‐induced extracellular matrix accumulation, oxidative stress, and inflammation in human glomerular mesangial cells

Cited by 36 publications

References 27 publications

Eriodictyol Attenuates MCAO-Induced Brain Injury and Neurological Deficits via Reversing the Autophagy Dysfunction

Eriodictyol Attenuates MCAO-Induced Brain Injury and Neurological Deficits via Reversing the Autophagy Dysfunction

Transcriptomic Analysis Reveals the Protection of Astragaloside IV against Diabetic Nephropathy by Modulating Inflammation

HMGB1 mediates lipopolysaccharide-induced inflammation via interacting with GPX4 in colon cancer cells

Contact Info

Product

Resources

About