Browsing by Subject "Nrf2"

Now showing 1 - 3 of 3
  • Thumbnail Image
    Publication
    Open Access
    Electroacupuncture pretreatment inhibits ferroptosis and inflammation after middle cerebral artery occlusion in rats by activating Nrf2
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Pu, Yanpeng; Cheng, Jingyan; Wang, Zhenya; Zhang, Jingbo; Liang, Fajun; Zhang, Xianbao; Zheng, Zhijun; Yin, Miaomiao; Wang, Zhen
    Objective. Electroacupuncture (EA) pretreatment can effectively increase the tolerance of the brain to ischemic stroke. The mechanism of ischemic tolerance induced by EA is related to Nrf2, but its specific mechanism has not been elucidated. This paper was designed to explore the effect of EA pretreatment on brain injury and the related mechanisms. Methods. Rats were pretreated with EA before middle cerebral artery occlusion (MCAO) modeling. The symptoms of neurological deficit and the volume of cerebral infarction were measured. The levels of inflammatory factors, oxidative stress-related factors, LPO, ROS, and Fe2+ were evaluated by the corresponding kits. Cell apoptosis was determined through TUNEL staining. The mRNA expression of inflammatory factors was examined by RT-qPCR, and the protein expression of ferroptosis-related factors, pyroptosis-related proteins, Keap1, Nrf2, HO-1, and NQO1 by western blotting. Results. EA pretreatment improved the symptoms of neurological deficit and reduced the volume of cerebral infarction. EA pretreatment significantly inhibited oxidative stress, inflammatory response, ferroptosis, pyroptosis, and apoptosis in brain tissues of MCAO rats. Mechanistically, EA pretreatment could activate Nrf2 expression and reduce Keap1 expression. Conclusion. EA pretreatment reduced inflammation and oxidative stress and inhibited ferroptosis by activating Nrf2 expression, ultimately delaying the development of ischemic stroke.
  • Thumbnail Image
    Publication
    Open Access
    Lysimachia christinae Hance aqueous extract ameliorates renal injury in kidney stone rats and calcium oxalate crystal-induced oxidative stress in HK-2 cells via inhibiting the PI3K/Akt/mTOR pathway
    (2026) Shengni Lv; Wangen Wang; Liangrong Zhu; Luning Lin; Xintian Zheng; Biología Celular e Histología
    Objectives. Kidney stones are a frequent urinary system disorder. Lysimachia christinae Hance is an accepted herb in traditional Chinese medicine for treating kidney stones. However, the effects and mechanisms of Lysimachia christinae Hance aqueous extract (LCH) are yet to be elucidated. Methods. The function of the aqueous extract of LCH was assessed using kidney stone rat models induced by 1% ethylene glycol+2% NH4Cl. Additionally, an in vitro model of human renal tubular epithelial cells (HK-2) treated with calcium oxalate was used. Results. Resultantly, the treatment of aqueous extract of LCH at different concentrations or LCH+LY294002 (PI3K-specific inhibitor) showed significant improve ment in inorganic ions and renal pathological injury in nephrolithiasis rats. Besides, consistent with the in vivo assay, LCH-containing serum increased cell viability and inhibited oxidative stress and deposition of Ca2+ in HK 2 cells, while the influences of LCH-containing serum were attenuated. Mechanistically, the aqueous extract of LCH and LCH-containing serum also promoted Nrf2 and HO-1 levels and inhibited the phosphorylated expression levels of PI3K, AKT, and mTOR. Conclusion. This study shows that LCH ameliorates the kidney damage in kidney stone rats and HK-2 cells. The mechanism of LCH in treating kidney stones is related to the activation of the Nrf2/HO-1 axis and the inhibition of the PI3K/Akt/mTOR pathway.
  • Thumbnail Image
    Publication
    Open Access
    Pinocembrin ameliorates non-alcoholic fatty liver disease by activating Nrf2/HO-1 and inhibiting the NF-κB signaling pathway
    (Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Chen Weina; Xue Diming; Feng Xia; Zhong Yinhang; Li Quanqing; Zhang Weihang; Jiang Guojun; Biología Celular e Histología
    Objectives. The high intake of high-fat diets and changes in sedentary lifestyles have led to an increase in non-alcoholic fatty liver disease (NAFLD). This study aimed to investigate the effect and mechanism of Pinocembrin (Pin) on NAFLD in vivo and in vitro. Methods. The pharmacodynamics of Pin alone or in combination with ML385 was assessed in high-fat diet (HFD)-mediated NAFLD mice. HepG2 cells were treated with palmitic acid (PA)/oleic acid (OA) (1:2) as an in vitro model to study the effect of Pin on lipid deposition and oxidative stress. The roles of Pin in glucose and lipid metabolism, inflammation, oxidative stress, and the Nrf2/HO-1/NF-κB pathway were measured. Results. Pin alleviated lipid deposition, inflam-matory response, and oxidative stress in HFD-induced NAFLD mice and PA/OA-induced HepG2 cells. Moreover, ML385 partly attenuated the protection of Pin on inflammatory response and oxidative stress in vivo and in vitro. More importantly, feeding with an HFD significantly decreased the expression of Nrf2 and HO-1, but treatment with Pin increased their expression, accompanied by an increased nuclear transposition of Nrf2. Conclusion. Taken together, these results indicated that Pin alleviated glucose and lipid metabolism disorders, inflammation, and oxidative stress in NAFLD by activating the Nrf2/HO-1 signaling pathway and restraining the NF-κB pathway