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WAC alleviated adriamycin‐induced apoptosis in vitro. (a, b) The effect of adriamycin on apoptosis of NRK‐52E. NRK‐52E cells in the 6‐well plate were treated with challenged with diverse levels of adriamycin (0, 0.25, 0.5, and 1 μg/ml) for 24 hr, and the cell apoptotic were identified using flow cytometry by labeling the Annexin V‐FITC/PI(A) and using TUNEL and DAPI staining. (c, d) The effects of WAC on adriamycin‐induced apoptosis in NRK‐52E cells. NRK‐52E cells were treated with adriamycin (1 μg/ml) and WAC (4 mg/ml) for 24 hr. The cell apoptosis was detected using TUNEL and DAPI dying, and the expression of Bcl‐2, Bax, caspase‐3, and cleaved caspase‐3 were identified using immunoblotting. The dyed cells were studied using a fluorescence microscope device (200×). The quantitative measurements of the fluorescence intensities were completed using the ImageJ program. Semi‐quantitative densitometry analysis was performed to measure the expression of apoptosis markers, and the ratios of Bax/Bcl‐2 and cleaved caspase‐3/caspase‐3 are shown as unique figures. Data are presented as means ± SD; n = 3/group. ##p < .01 compared to the ADR group. **p < .01 compared to the control group. Scale bar = 50 µm
Source publication
Artemisia capillaris Thunb. is widely used in the treatment of kidney diseases, but the underlying mechanism remain elusive. Therefore, this study aimed to elucidate the mechanism of Artemisia capillaris Thunb. in alleviating renal injury. And renoprotective effects of freeze-dried powder of Artemisia capillaris Thunb. water extract (WAC) were asse...
Citations
... Yinchen extract (HACE) can protect the kidneys of diabetic rats, so Aiye and Yinchen can protect the kidneys and liver in the process of RTI. 12 Sesquiterpene lactones are mainly isolated from Asteraceae species, which were found in seven Artemisia species collected from Tajikistan, and exhibit the biological effects of inhibiting severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). 13,14 As a whole, Artemisia species displays pharmacological effects in the prevention and treatment of RTI, but more research is needed to determine the underlying pharmacological processes. ...
Objective: To study the mechanism of Artemisia in the treatment of respiratory tract infection (RTI) by network pharmacology and molecular docking. Methods: The active constituents and targets of Artemisia were screened by the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP). Gene Cards database to obtain disease targets associated with RTI. The key targets of intersection were used to construct the protein–protein interaction (PPI) network, and the hub gene was obtained through topological analysis to construct the pharmacology regulation network of traditional Chinese medicine. The key targets were analyzed by R language enrichment, and the regulatory network diagram of the key target function/pathway was constructed. Molecular docking verifies the binding of the drug to the target predicted by network pharmacology. Results: 144 active components of Artemisia regulated 133 target proteins related to RTI, the core components were β-sitosterol, quercetin, isorhamnetin, artemisinin, etc. Gene ontology enrichment analysis showed that Artemisia regulates receptor ligand activity, cytokine activity, and other molecular functions by acting on membrane region, membrane raft and other cellular structures in the treatment of RTI, thus affecting biological processes such as the response to drugs and bacteria-derived molecules. Kyoto Encyclopedia of Genes and Genomes enrichment analysis indicated that phosphatidylinositol 3-kinase (PI3K)-protein kinase B (Akt), tumor necrosis factor, interleukin-17 (IL-17) signaling pathway was the main pathway for RTI treatment. The molecular docking method confirmed the high affinity between the active ingredient and the RTI target. Conclusions: Artemisia species, a multitarget medication, has been shown to be a viable therapy option for RTI by network pharmacology techniques based on data mining and molecular docking approaches.
... Adriamycin (generic name is doxorubicin (DOX)) is an anthracycline group antineoplastic agent that induces nephropathy experimentaly 6,7 . In the adriamycin-induced nephrotic syndrome model, adriamycin stimulates oxidative damage in the glomeruli, increases podocyte damage, causes glomerular basement membrane changes, and creates minimal change disease/focal segmental glomerulosclerosis-like damage 8,9 . An adriamycininduced nephropathy model is induced by a single tail vein injection of 5-7.5 mg/kg adriamycin 10 . ...
Introduction:
Nephrotic syndrome (NS) is one of the reasons of end-stage kidney disease, and elucidating the pathogenesis and offer new treatment options is important. Oxidative stress might trigger pathogenesis systemically or isolated in the kidneys. Octreotide (OCT) has beneficial antioxidant effects. We aimed to investigate the source of oxidative stress and the effect of OCT on experimental NS model.
Methods:
Twenty-four non-uremic Wistar albino rats were divided into 3 groups. Control group, 2 mL saline intramuscular (im); NS group, adriamycin 5 mg/kg intravenous (iv); NS treatment group, adriamycin 5 mg/kg (iv) and OCT 200 mcg/kg (im) were administered at baseline (Day 0). At the end of 21 days, creatinine and protein levels were measured in 24-hour urine samples. Erythrocyte and renal catalase (CAT) and thiobarbituric acid reactive substance (TBARS) were measured. Renal histology was also evaluated.
Results:
There was no significant difference among the 3 groups in terms of CAT and TBARS in erythrocytes. Renal CAT level was lowest in NS group, and significantly lower than the control group. In treatment group, CAT level significantly increased compared with NS group. In terms of renal histology, tubular and interstitial evaluations were similar in all groups. Glomerular score was significantly higher in NS group compared with control group and it was significantly decreased in treatment group compared to NS group.
Conclusions:
Oxidative stress in NS might be due to the decrease in antioxidant protection mechanism in kidney. Octreotide improves antioxidant levels and histology in renal tissue and might be a treatment option.
... A adriamicina (cujo nome genérico é doxorrubicina (DOX)) é um agente antineoplásico do grupo das antraciclinas que induz a nefropatia experimentalmente 6,7 . No modelo de síndrome nefrótica induzida por adriamicina, a adriamicina estimula o dano oxidativo nos glomérulos, aumenta o dano aos podócitos, causa alterações na membrana basal glomerular e provoca danos semelhantes à doença de alteração mínima/glomeruloesclerose segmentar focal 8,9 . Um modelo de nefropatia induzida por adriamicina é induzido por uma única injeção na veia caudal de 5-7,5 mg/kg de adriamicina 10 . ...
Resumo Introdução: Síndrome nefrótica (SN) é uma das causas de doença renal em estágio terminal. É importante elucidar a patogênese e oferecer novas opções de tratamento. Estresse oxidativo pode desencadear a patogênese sistemicamente ou isoladamente nos rins. O octreotide (OCT) tem efeitos antioxidantes benéficos. Nosso objetivo foi investigar a fonte de estresse oxidativo e efeito do OCT no modelo experimental de SN. Métodos: Dividimos 24 ratos albinos Wistar não urêmicos em 3 grupos. Grupo controle, 2 mL de solução salina intramuscular (im); grupo SN, adriamicina 5 mg/kg intravenosa (iv); grupo tratamento SN, adriamicina 5 mg/kg (iv) e OCT 200 mcg/kg (im) foram administrados no início do estudo (Dia 0). Aos 21 dias, mediram-se os níveis de creatinina e proteína em amostras de urina de 24 horas. Mediu-se a catalase (CAT) eritrocitária e renal e a substância reativa ao ácido tiobarbitúrico (TBARS). Avaliou-se também histologia renal. Resultados: Não houve diferença significativa entre os três grupos em termos de CAT e TBARS em eritrócitos. O nível de CAT renal foi menor no grupo SN e significativamente menor que no grupo controle. No grupo tratamento, o nível de CAT aumentou significativamente em comparação com o grupo SN. Quanto à histologia renal, as avaliações tubular e intersticial foram semelhantes em todos os grupos. O escore glomerular foi significativamente maior no grupo SN em comparação com o grupo controle e diminuiu significativamente no grupo de tratamento em comparação com o grupo SN. Conclusões: Estresse oxidativo na SN pode ser devido à diminuição do mecanismo de proteção antioxidante nos rins. O octreotide melhora níveis de antioxidantes e histologia do tecido renal e pode ser uma opção de tratamento.
... The decoction was collected. The decoction solution collected twice was mixed, and the decoction solution was filtered, centrifuged to remove insoluble substances, and lyophilized at -50°C for 48 h to a powdered solid (Huang et al., 2022). The average yield of AC was 15.6% (W/W). ...
Non-alcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases and is a nutritional metabolic disease. Artemisia capillaris (AC) is the above-ground dried part of Artemisia capillaris Thunb. or Artemisia scoparia Waldst. et Kit. , a natural medicinal plant with pharmacological effects of heat-clearing and biliary-promoting. In order to evaluate the therapeutic effect of Artemisia capillaris on NAFLD and obesity, experiments were conducted using aqueous extracts of Artemisia capillaris (WAC) to intervene in NAFLD models in vivo and in vitro . In vivo experiments were performed using HFD-fed (high fat diet) C57BL/6 mice to induce NAFLD model, and in vitro experiments were performed using oleic acid to induce HepG2 cells to construct NAFLD cell model. H.E. staining and oil red O staining of liver tissue were used to observe hepatocytes. Blood biochemistry analyzer was used to detect serum lipid levels in mice. The drug targets and mechanism of action of AC to improve NAFLD were investigated by western blotting, qRT-PCR and immunofluorescence. The results showed that C57BL/6 mice fed HFD continuously for 16 weeks met the criteria for NAFLD in terms of lipid index and hepatocyte fat accumulation. WAC was able to reverse the elevation of serum lipid levels induced by high-fat diet in mice. WAC promoted the phosphorylation levels of PI3K/AKT and AMPK in liver and HepG2 cells of NAFLD mice, inhibited SREBP-1c expression, reduced TG and lipogenesis, and decreased lipid accumulation. In summary, WAC extract activates PI3K/AKT pathway, reduces SREBP-1c protein expression by promoting AMPK phosphorylation, and decreases fatty acid synthesis and TG content in hepatocytes. AC can be used as a potential health herb to improve NAFLD and obesity.
... However, the impact of ferroptosis on the development of ADR-induced renal damage has not been elucidated. Diverse ROS scavengers have been shown to alleviate Adriamycin-induced nephrotoxicity in rats (Liu et al., 2018;Amarasiri et al., 2020;Huang et al., 2022). Astragaloside IV (ASIV) has been found to inhibit Adriamycin-induced ferroptosis in the heart in addition to the antioxidant function in our previous research (Luo et al., 2021a). ...
Adriamycin (ADR) has been utilized to treat cancer for several decades. However, ADR-induced renal injury is one of the most common side effects accompanying ADR therapy. In the present study, we revealed that astragaloside IV (ASIV) was beneficial for renal injury caused by Adriamycin. We demonstrated that ASIV significantly ameliorated kidney injury, improved renal dysfunction, reduced oxidative stress, alleviated iron accumulation, and inhibited the induction of ferroptosis by ADR. ASIV also rescued the intracellular levels of nuclear factor-erythroid-2-related factor 2 (Nrf2) and promoted nuclear translocation of Nrf2. These protective effects of ASIV on renal injury might be attained through the ASIV-induced activation of the Pi3K/Akt signaling pathway. In vitro, the treatment of the HK-2 cells with fer-1 or deferoxamine mesylate obviously improved cell viability during Adriamycin administration. On the other hand, the protective role of ASIV can be abrogated by RSL3 to some extent. Moreover, ASIV lowered the expression of transferrin receptor 1 and divalent metal transporter 1 while enhancing the expression of ferropotin 1 and glutathione peroxidase 4 in ADR administrated cells, the effects of which were akin to those of deferoxamine mesylate. Furthermore, ASIV increased the phosphorylation of Pi3K, Akt, and the expression of Nrf2 and glutathione peroxidase 4 compared to HK-2 cells stimulated by ADR. However, Pi3K inhibitor LY294002 abrogated these activations. In conclusion, ferroptosis may involve in ADR-induced nephrotoxicity, and ASIV might protect nephrocytes against ADR-induced ferroptosis, perhaps via activations of the Pi3K/Akt and Nrf2 signaling pathways.
