Aristolochic acid A是一种从马兜铃科植物（Aristolochia debilis Sieb. et Zucc.）中提取的天然产物，强烈引起卵巢成熟过程中通过抑制Akt磷酸化介导的凋亡抑制的毒性损伤。
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Aristolochic Acid A (Aristolochic acid I), is the main component of plant extract Aristolochic acids, which are found in various herbal plants of genus Aristolochia and Asarum, strongly induces toxic damage during ovarian maturation by inhibiting Akt phosphorylation-mediated suppression of apoptosis. Aristolochic acid A (150, 200 μM, 24 hours) inhibits the cell viabilities of kidney cells HEK293 and HK-2. Aristolochic acid A (100, 200 μM, 24 hours) causes a concentration-dependent decrease in bladder cancer-associated protein (BLCAP) mRNA levels in kidney cells (HEK 293 and HK-2), and bladder cancer cell line (HT-1376). Aristolochic acid A (100, 200 μM, 24 hours) weakens the BLCAP protein signals in a dose-dependent manner in both HEK293 and HT-1376 cells[3]. AA (Aristolochic Acid A) has been found to damage broilers' kidneys by breaking the redox balance to form oxidative stress, along with promoting apoptosis of renal cells[4]. Additionally, AAI promoted apoptosis in SSCs, which was accompanied by upregulation of caspase 3, P53 and BAX expression and downregulation of Bcl-2 expression, and suppressed autophagy, which was accompanied by upregulation of P62 expression and downregulation of ATG5 and LC3B expression, in a concentration-dependent manner. AAI (Aristolochic acid I) impaired spermatogenesis in rats, as identified by degeneration of the seminiferous epithelium, and increased apoptosis of testicular cells[5]. The mechanism of AA-I-induced hepatotoxicity was associated with oxidative-stress-mediated apoptosis and mitochondrial damage[6].
Aristolochic acid A/马兜铃酸A 细胞实验
Cell Line
Concentration
Treated Time
Description
References
Bone marrow-derived macrophages (BMDMs)
10 mg/ml
0, 6, 12, 24, 48 hours
To study the effect of AA on macrophage polarization, results showed that AA treatment significantly increased the expression of M2-related genes.
Front Immunol. 2022 May 2;13:864984.
Raw264.7 cells
10 mg/ml
0, 6, 12, 24, 48 hours
To study the effect of AA on macrophage polarization, results showed that AA treatment significantly increased the expression of M2-related genes.
Front Immunol. 2022 May 2;13:864984.
Rat liver microsomes
10 µM
20 min
Investigation of AAI O-demethylation, identifying CYP1A and CYP2C subfamily as major catalysts
Int J Mol Sci. 2015 Nov 18;16(11):27561-75.
Human liver microsomes
10 µM
20 min
Investigation of AAI O-demethylation, identifying CYP1A1/2 and CYP3A4 as major catalysts
Int J Mol Sci. 2015 Nov 18;16(11):27561-75.
HEK293 cells
20 µM
24 hours
To validate KLF15 binding sites in the CPT1A and ACAA2 promoter regions by chromatin immunoprecipitation assay. Results showed that KLF15 binding to these promoter regions was maintained even after AAI treatment.
Kidney Int. 2021 Dec;100(6):1250-1267.
HK-2 cells
20 µM
24 hours
To evaluate the protective effect of KLF15 overexpression on AAI-induced cell injury. Results showed that KLF15 overexpression partially rescued the loss of FAO in AAI-treated cells.
Kidney Int. 2021 Dec;100(6):1250-1267.
NRK52E cells
40 µM
24 hours
To investigate the ameliorative effect of LYC on AAI-induced renal fibrosis and its mechanism. The results showed that LYC intervention activated mitophagy, reduced AAI-induced mitochondrial damage, and improved renal fibrosis by inhibiting the AKT signaling pathway.
Autophagy. 2024 May;20(5):1114-1133.
Human renal proximal tubular epithelial cell line (HK-2)
100 µM
24 hours
Evaluate the inhibitory effect of AAI on cell proliferation and DNA damage, SFII significantly alleviated AAI-induced DNA damage and apoptosis.
Acta Pharmacol Sin. 2023 Jul;44(7):1429-1441.
Human normal liver cell line (L02)
20 µM, 50 µM
24 hours, 48 hours
Evaluate the inhibitory effect of AAI on cell proliferation and DNA damage, SFII significantly alleviated AAI-induced DNA damage and apoptosis.
Acta Pharmacol Sin. 2023 Jul;44(7):1429-1441.
HK-2 cells
5 µM and 10 µM
4 hours
To study AAI-induced mitochondrial acidification, results showed increased mitochondrial acidification with higher AAI concentrations.
Mater Today Bio. 2024 Sep 11;28:101240.
Supersomes™ (recombinant CYP enzymes expressed in insect cells)
10 µM
Evaluation of cytochrome b5 effect on AAI oxidation, identifying human CYP1A1 and 1A2 as major enzymes for AAI oxidation
Int J Mol Sci. 2015 Nov 18;16(11):27561-75.
Aristolochic acid A/马兜铃酸A 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Sprague-Dawley rats
Hepatocellular carcinoma model
Oral
0.1, 1, or 10 mg/kg
5 days a week for 6 weeks (medium-term study) or 52 weeks (long-term study)
To evaluate the tumor-initiating or -promoting activity of AAI. Results showed that high-dose AAI (10 mg/kg) promoted clonal expansion but did not induce HCC.
Acta Pharmacol Sin. 2021 Dec;42(12):2094-2105
C57BL/6 mice
AAI-induced renal fibrosis model
Oral gavage
10 mg/kg
Once daily for 28 days
To investigate the ameliorative effect of LYC on AAI-induced renal fibrosis and its mechanism. The results showed that LYC intervention alleviated AAI-induced renal histopathological damage, restored renal function, and improved renal fibrosis by inhibiting the TGFB signaling pathway and activating mitophagy.
Autophagy. 2024 May;20(5):1114-1133.
Mice
AAN model
Intraperitoneal injection
10 mg/kg
1, 3, 7, 14, 28 days
To study AA-induced renal fibrosis, results showed that AA treatment significantly increased renal fibrosis and macrophage M2 polarization.
Front Immunol. 2022 May 2;13:864984.
C57BL/6J mice
AAI-induced acute kidney injury model
Intraperitoneal injection
10 mg/kg
Single injection, sacrificed after 3 days
To study the role of PSTPIP2 in AAI-induced acute kidney injury, it was found that conditional knock-in of Pstpip2 alleviated kidney injury and apoptosis.
Elife. 2024 Feb 5;13:e89740
C57BL/6 mice
AAI-induced hepatotoxicity Mice model
Intraperitoneal injection
2 mg/kg
Once daily for 4 weeks or 8 weeks
To investigate the mechanisms of AAI-induced hepatotoxicity, results showed that AAI exposure led to body weight loss, liver injury, inflammatory cell infiltration, and increased levels of ALT and AST.
Precis Clin Med. 2022 Sep 22;5(4):pbac023
C57 BL/6 mice
AA-induced nephrotoxicity model
Intraperitoneal injection
2 mg/kg
Once a day for 4 weeks
Evaluate AA-induced nephrotoxicity and metabolic disorders
Int J Biol Sci. 2022 Feb 21;18(5):2003-2017
Sprague-Dawley rats
Hepatocellular carcinoma model
Oral
20, 50, or 100 mg/kg
Single dose
To evaluate the tumor-initiating or -promoting activity of AAI. Results showed that high-dose AAI (10 mg/kg) promoted clonal expansion but did not induce HCC.
Acta Pharmacol Sin. 2021 Dec;42(12):2094-2105
Mice
AAI-induced nephrotoxicity model
Tail vein injection
200 μM
Five times per week for two weeks
To study AAI-induced nephrotoxicity and mitochondrial acidification, results showed AAI caused renal injury and mitochondrial acidification, which was mitigated by LC co-treatment.
Mater Today Bio. 2024 Sep 11;28:101240.
C57BL/6 mice
Klf15PTKO mice
Intraperitoneal injection
3 mg/kg
Every 3 days for 2 weeks
To evaluate the effect of PT-specific KLF15 deletion on AAI-induced kidney injury. Results showed that Klf15PTKO mice exhibited more severe tubular injury and kidney function decline after AAI treatment.
Kidney Int. 2021 Dec;100(6):1250-1267.
C57BL/6 mice
AAN model
Intraperitoneal injection
3 mg/kg
Twice a week for 4 weeks followed by 4 weeks of remodeling time
To investigate whether AA induces renal aging, results showed AA caused renal atrophy, tubulointerstitial fibrosis, and renal functional decline, accompanied by increased renal p16 mRNA expression and SA-β-gal activity
Int J Mol Sci. 2021 Nov 18;22(22):12432
Mice
Trp53(+/+), Trp53(+/-), and Trp53(-/-) mice
Intraperitoneal injection
3.5 mg/kg
Daily for six days
To investigate the impact of p53 on AAI-induced gene expression in vivo, results showed that AAI significantly altered gene expression in kidneys of Trp53(+/+), Trp53(+/-), and Trp53(-/-) mice
Int J Mol Sci. 2019 Dec 6;20(24):6155
C57BL/6 mice
Acute renal injury model and renal fibrosis model
Intraperitoneal injection
5 mg/kg, 10 mg/kg
Three consecutive days or 14 days after a single dose
Evaluate the protective effect of SFII on AAI-induced renal injury and fibrosis, SFII effectively attenuated acute renal injury and fibrosis caused by AAI in vivo.
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