Baicalin improves podocyte injury in rats with diabetic nephropathy by inhibiting PI3K/Akt/mTOR signaling pathway

Ou, Yi-Hung; Zhang, Wenjuan; Chen, Shaopeng; Hai-hua, Deng

doi:10.1515/med-2021-0335

Cited by 18 publications

(15 citation statements)

References 30 publications

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“…Consistent with our findings, Ou et al revealed that BA attenuated podocyte damage in DN rats partially via the suppression of inflammatory responses and oxidative stress by inactivating the PI3K/Akt/mTOR pathway. 11 As demonstrated by Yang et al, BA might improve renal function and delay disease progression in DN through its anti-inflammatory and anti-oxidative properties. 13 Ma et al reported that BA treatment suppressed inflammation and oxidative stress in DN by inhibiting the MAPK and Nrf2 signaling.…”

Section: Discussionmentioning

confidence: 95%

“… 9 BA protects against fluoxetine-induced hepatic injury by repressing inflammation and oxidative stress. 10 BA has also been found to alleviate the progression of DN by relieving podocyte injury, 11 diminishing renal fibrosis, 12 and improving renal function. 13 Moreover, BA exerts a renoprotective role in DN by suppressing inflammation and oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

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Baicalin Exerts a Protective Effect in Diabetic Nephropathy by Repressing Inflammation and Oxidative Stress Through the SphK1/S1P/NF-κB Signaling Pathway

Ren¹,

Jiao²,

Yan³

et al. 2023

DMSO

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Background: Inflammation and oxidative stress contribute to the development of diabetic nephropathy (DN). Baicalin (BA) shows renal protection against DN through its anti-inflammatory and anti-oxidant properties. However, the molecular mechanism by which BA exerts the therapeutic effects on DN remains to be investigated. Methods: The db/db mice and high glucose (HG)-induced HK-2 cells were used as the in vivo and in vitro model of DN, respectively. The effects of BA were assessed by detecting the related blood and urine biochemical parameters, kidney histopathology, inflammatory cytokine production, oxidative stress indicators, and apoptosis. Cell viability and apoptosis were detected by CCK-8 assay and TUNEL assay, respectively. Related protein levels were measured by an immunoblotting method. Results: In db/db model mice, BA reduced serum glucose concentration, decreased blood lipid levels, ameliorated kidney functions, and decreased histopathological changes in kidney tissues. BA also alleviated oxidative stress and inflammation in db/db mice. In addition, BA blocked the activation of sphingosine kinases type 1/sphingosine 1-phosphate (SphK1/S1P)/NF-κB pathway in db/db mice. In HK-2 cells, BA hindered HG-induced apoptosis, oxidative stress and inflammation, while overexpression of SphK1 or S1P could reverse these effects. BA alleviated HG-induced apoptosis, oxidative stress and inflammation in HK-2 cells through the S1P/NF-κB pathway. Furthermore, BA blocked the NF-κB signaling by diminishing p65 nuclear translocation via the SphK1/S1P pathway. Conclusion: Our study strongly suggests that BA protects against DN via ameliorating inflammation, oxidative stress and apoptosis through the SphK1/S1P/NF-κB pathway. This study provides a novel insight into the therapeutic effects of BA in DN.

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Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

Baicalin Exerts a Protective Effect in Diabetic Nephropathy by Repressing Inflammation and Oxidative Stress Through the SphK1/S1P/NF-κB Signaling Pathway

Ren¹,

Jiao²,

Yan³

et al. 2023

DMSO

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“…It was found that chondrocyte apoptosis decreased, autophagy increased, and the severity of OA was alleviated in mice with mTOR knockout (Zhang et al, 2015). A growing body of evidence shows that Baicalin can regulate PI3K/AKT/mTOR pathway, which can protect podocytes from injury induced by high glucose and activate macrophage autophagy to play an antimycobacterial and anti‐inflammatory role (Ou et al, 2021; Zhang et al, 2017). In this study, we confirmed that Baicalin can promote chondrocyte autophagy by inhibiting the activation of PI3K/AKT/mTOR pathway.…”

Section: Discussionmentioning

confidence: 99%

Baicalin mitigated IL‐1β‐Induced osteoarthritis chondrocytes damage through activating mitophagy

2023

Chem Biol Drug Des

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Mitophagy is related to chondrocyte homeostasis and plays a key role in the progress of osteoarthritis (OA). Baicalin has a protective effect on OA chondrocytes, the aim of this study was to explore whether the effect of Baicalin on IL-1β-induced chondrocyte injury is related to the regulation of mitophagy. The expression of collagen II in chondrocytes was detected to identify chondrocytes. The effects of different concentrations of Baicalin (10, 20 and 40 μM), autophagy inhibitor (3-Methyladenine), autophagy activator (rapamycin) and Baicalin combined with PI3K agonist (740Y-P) on the viability (cell counting kit 8), apoptosis (flow cytometry), autophagy activation (Monodansylcadaverine staining) and mitochondrial membrane potential (JC-1 kit) of IL-1β-induced chondrocytes were evaluated. The co-localization of autophagosome and mitochondria was determined by immunofluorescence. Apoptosis-, autophagy-, PI3K/AKT/mTOR pathway-and mitophagyrelated proteins were detected by western blot. Our result revealed that Baicalin and rapamycin facilitated cell viability, autophagy and mitophagy, elevated mitochondrial membrane potential and suppressed apoptosis of IL-1β-induced rat chondrocytes. In addition, Baicalin and rapamycin upregulated the levels of Bcl-2, Beclin 1, LC3-II/LC3-I, p-Drp1, PINK1 and Parkin as well as downregulated the levels of Bax, cleaved caspase-3, P62, p-PI3K/PI3K, p-mTOR/mTOR and Drp1 in IL-1β-induced rat chondrocytes. However, 3-Methyladenine did the opposite effects of Baicalin and 740Y-P reversed the effects of Baicalin on IL-1β-induced rat chondrocytes. In conclusion, Baicalin activated mitophagy in IL-1β-induced chondrocytes by inhibiting PI3K/AKT/mTOR pathway and activating PINK1/Parkin and PINK1/Drp-1 pathway, thereby reducing the chondrocyte injury.

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“…Baicalin ( Figure 2 e) ameliorated diabetic conditions in db/db mice by alleviating oxidative stress and inflammation, and its underlying mechanisms were associated with the activation of the Nrf2-mediated antioxidant signaling pathway and the inhibition of the MAPK-mediated inflammatory signaling pathway [ 166 ]. Baicalin protected podocytes by downregulating the activity of the PI3K/AKT/mammalian target of rapamycin (mTOR) signaling pathway in STZ-induced DN rats [ 159 ]. Baicalin could also alleviate renal injury in STZ-induced DN mice through restoring Klotho expression and inhibiting Klotho hypermethylation to counter TGF-β1 signaling [ 164 ].…”

Section: Flavonoids In Ckdmentioning

confidence: 99%

Flavonoids in Treatment of Chronic Kidney Disease

et al. 2022

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Chronic kidney disease (CKD) is a progressive systemic disease, which changes the function and structure of the kidneys irreversibly over months or years. The final common pathological manifestation of chronic kidney disease is renal fibrosis and is characterized by glomerulosclerosis, tubular atrophy, and interstitial fibrosis. In recent years, numerous studies have reported the therapeutic benefits of natural products against modern diseases. Substantial attention has been focused on the biological role of polyphenols, in particular flavonoids, presenting broadly in plants and diets, referring to thousands of plant compounds with a common basic structure. Evidence-based pharmacological data have shown that flavonoids play an important role in preventing and managing CKD and renal fibrosis. These compounds can prevent renal dysfunction and improve renal function by blocking or suppressing deleterious pathways such as oxidative stress and inflammation. In this review, we summarize the function and beneficial properties of common flavonoids for the treatment of CKD and the relative risk factors of CKD.

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Baicalin improves podocyte injury in rats with diabetic nephropathy by inhibiting PI3K/Akt/mTOR signaling pathway

Cited by 18 publications

References 30 publications

Baicalin Exerts a Protective Effect in Diabetic Nephropathy by Repressing Inflammation and Oxidative Stress Through the SphK1/S1P/NF-κB Signaling Pathway

Baicalin Exerts a Protective Effect in Diabetic Nephropathy by Repressing Inflammation and Oxidative Stress Through the SphK1/S1P/NF-κB Signaling Pathway

Baicalin mitigated IL‐1β‐Induced osteoarthritis chondrocytes damage through activating mitophagy

Flavonoids in Treatment of Chronic Kidney Disease

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