ArticleAging2022
Renoprotective effect of Tanshinone IIA against kidney injury induced by ischemia-reperfusion in obese rats.
Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Investigating the Mechanisms ofACS omega · 2026Article
- Pathological triad of perioperative acute kidney injury: renal microcirculatory hypoxia, mitochondrial damage, and immuno-metabolic reprogramming.Frontiers in immunology · 2026Review
- Tanshinone IIA prevents septicemia acute kidney injury via regulating the DUSP10/JNK/P38/NLRP3 pathway.American journal of translational research · 2026Article
- Exploring Chinese Herbal Medicines for Acute Kidney Injury: Pharmacological Mechanisms and Clinical Potential.Drug design, development and therapy · 2026Review
- Tanshinone IIA alleviates LPS-induced acute kidney injury by inhibiting RIP3/Nrf2-mediated oxidative stress.Renal failure · 2025Article
- Mechanism of PI3K/Akt‑mediated mitochondrial pathway in obesity‑induced apoptosis (Review).Biomedical reports · 2025Review
- Nephroprotective effects of substances of medicine food homology and traditional Chinese medicine phytochemicals against acute kidney injury.Frontiers in pharmacology · 2025Review
- Rodent models of AKI and AKI-CKD transition: an update in 2024.American journal of physiology. Renal physiology · 2024Review
- Diallyl trisulfide improves spinal cord ischemia-reperfusion injury damage by activating AMPK to stabilize mitochondrial function.Journal of orthopaedic surgery and research · 2023Article
- Renoprotective Effects of Tanshinone IIA: A Literature Review.Molecules (Basel, Switzerland) · 2023Review
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveObesity enhances the frequency and severity of acute kidney injury (AKI) induced by renal ischemia-reperfusion (IR). Tanshinone IIA (TIIA) pre-treatment was used to alleviate renal injury induced by renal IR, and whether TIIA can attenuate renal cell apoptosis via modulating mitochondrial function through PI3K/Akt/Bad pathway in obese rats was examined.
methodsMale rates were fed a high-fat diet for 8 weeks to generate obesity, followed by 30 min of kidney ischemia and 24 h reperfusion induced AKI. The male obese rates were given TIIA (5 mg/kg.d, 10 mg/kg.d, and 20 mg/kg.d) for 2 weeks before renal IR.
resultsTIIA alleviated the pathohistological injury and apoptosis induced by IR. In addition, TIIA improved renal function, inflammatory factor, and balance of oxidation and antioxidation in obese rats after renal IR. At the same time, TIIA can inhibit cell apoptosis by improving mitochondrial function through the PI3K/Akt/Bad pathway. Mitochondrial dysfunction was supported by decreasing intracellular ATP, respiration controlling rate (RCR), mitochondrial membrane potential (MMP), and mitochondrial respiratory chain complex enzymes, and by increasing ROS, the opening of mitochondrial permeability transition pore (mPTP), and the mtDNA damage. The injury to mitochondrial dynamic function was assessed by decreasing Drp1, and increasing Mfn1/2; and the injury of mitochondrial biogenesis was assessed by decreasing PGC-1, Nrf1, and TFam.
conclusionsRenal mitochondrial dysfunction occurs along with renal IR and can induce renal cell apoptosis. Obesity can aggravate apoptosis. TIIA can attenuate renal cell apoptosis via modulating mitochondrial function through PI3K/Akt/Bad pathway in obese rats.
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