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Long Li

Researcher at Fudan University

Publications -  32
Citations -  831

Long Li is an academic researcher from Fudan University. The author has contributed to research in topics: Kidney & Transplantation. The author has an hindex of 15, co-authored 30 publications receiving 655 citations. Previous affiliations of Long Li include Shanghai Jiao Tong University.

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The protective effect of baicalin against renal ischemia-reperfusion injury through inhibition of inflammation and apoptosis

TL;DR: Baicalin may attenuate renal ischemia-reperfusion injury by inhibiting proinflammatory responses and mitochondria-mediated apoptosis and these effects are associated with the TLR2/4 signaling pathway and mitochondrial stress.
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Resveratrol Alleviates Inflammatory Responses and Oxidative Stress in Rat Kidney Ischemia-Reperfusion Injury and H2O2-Induced NRK-52E Cells via the Nrf2/TLR4/NF-κB Pathway.

TL;DR: RSV inhibited inflammatory responses and improved renal function after renal IRI and exerts its greatest effects by blocking inflammatory responses, lowering oxidative stress, and reducing apoptosis via the Nrf2/TLR4/NF-κB pathway.
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Renal telocytes contribute to the repair of ischemically injured renal tubules.

TL;DR: Renal TCs protect against renal IRI via an inflammation‐independent pathway and that growth factors play a significant role in this mechanism, and may protect TECs in certain microenvironments while interacting with other cells.
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A novel proteolysis-resistant cyclic helix B peptide ameliorates kidney ischemia reperfusion injury

TL;DR: Thioether-cyclized helix B peptide was significantly stable in vivo and in vitro, and the phosphorylation of autophagy protein mTORC1 was dramatically reduced upon CHBP treatment, indicating that the novel metabolically stable CHBP is a promising therapeutic medicine for kidney IR injury treatment.
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Baicalin ameliorates H2O2 induced cytotoxicity in HK-2 cells through the inhibition of ER stress and the activation of Nrf2 signaling.

TL;DR: It is revealed that Baicalin pretreatment serves a protective role against H2O2-induced cytotoxicity in HK-2 cells, where the inhibition of ER stress and the activation of downstream Nrf2 signaling are involved.