Quercetin protected against isoniazide‐induced HepG2 cell apoptosis by activating the SIRT1/ERK pathway

Zhang, Yueming; Zhang, Wenrui; Tao, Lina; Zhai, Jinghui; Gao, Huan; Song, Yanqing; Qu, Xiaoyu

doi:10.1002/jbt.22369

Cited by 28 publications

(13 citation statements)

References 36 publications

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“…After SIRT1 silenced, the effect of curcumin was partially inhibited. This conclusion is consistent with many other studies, which had confirmed that isoniazid inhibited SIRT1 expression in HepG2 and HL7702 cells and downregulated SIRT1/PGC‐α/NRF1 pathway (Zhang, Li, et al, 2019; Zhang, Tang, et al, 2017; Zhang, Zhang, et al, 2019). Similarly, in 2018, Portale‐Perez DP's team found that, with SIRT1 inhibited, the activity of NAT2 increased; with SIRT1 stimulated, the result was quite opposite (Salazar‐Gonzalez et al, 2018; Turijan‐Espinoza et al, 2018).…”

Section: Discussionsupporting

confidence: 92%

Curcumin attenuates isoniazid‐induced hepatotoxicity by upregulating the SIRT1/PGC‐1α/NRF1 pathway

Luo

Chen

et al. 2022

J of Applied Toxicology

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As a serious infectious disease, tuberculosis threatens global public health. Isoniazid is the first-line drug not only in active tuberculosis but also in its prevention. Severe hepatotoxicity greatly limits its use. Curcumin, extracted from turmeric, has been found to relieve isoniazid-induced hepatotoxicity. However, the mechanism of isoniazid-induced hepatotoxicity and the protective effects of curcumin are not yet understood completely. We established both cell and animal models about isoniazidinduced hepatotoxicity and investigated the new mechanism of curcumin against isoniazid-induced liver injury. The experimental data in our study demonstrated that curcumin ameliorated isoniazid-mediated liver oxidative stress. The protective effects of curcumin were demonstrated and confirmed to be correlated with upregulating SIRT1/PGC-1α/NRF1 pathway. Western blot revealed that while inhibiting SIRT1 by the siRNA1 (a SIRT1 inhibitor), the expressions of SIRT1, PGC-1α/Ac-PGC-1α, and NRF1 decreased, and the protective effect that curcumin exerted on isoniazidtreated L-02 cells was significantly attenuated. Furthermore, curcumin improved liver functions and reduced necrosis of the isoniazid-treated BALB/c mice, accompanied by downregulating oxidative stress and inflammation in liver. Western blot revealed that curcumin treatment activates the SIRT1/PGC-1α/NRF1 pathway in the isoniazid-treated BALB/c mice. In conclusion, we found one mechanism of isoniazidinduced hepatotoxicity downregulating the SIRT1/PGC-1α/NRF1 pathway, and curcumin attenuated this hepatotoxicity by activating it. Our study provided a novel approach and mechanism for the treatment of isoniazid-induced hepatotoxicity.

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Section: Discussionsupporting

confidence: 92%

Curcumin attenuates isoniazid‐induced hepatotoxicity by upregulating the SIRT1/PGC‐1α/NRF1 pathway

Luo

Chen

et al. 2022

J of Applied Toxicology

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“…Quercetin (3,3 ,4 ,5,7-pentahydroxyflavone) is a flavonoid that is widely found in several foods, including grains, fruits, vegetables, and tea [8]. Quercetin has anti-inflammatory, anti-oxidant, and anti-apoptosis properties and thus, it recommended as a nutritional supplement for animals [9][10][11][12]. Moreover, quercetin can prevent oxidative stress by scavenging free radicals, removing oxidation products, and stimulating antioxidant enzymes in many animal models [13,14].…”

Section: Introductionmentioning

confidence: 99%

Quercetin Protects against Lipopolysaccharide-Induced Intestinal Oxidative Stress in Broiler Chickens through Activation of Nrf2 Pathway

Sun

Dong

et al. 2020

Molecules

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We investigated the potential ability of quercetin to protect against lipopolysaccharide (LPS)-induced intestinal oxidative stress in broiler chickens and the potential role of the Nrf2 (nuclear factor erythroid 2-related factor 2) signaling pathway. One-day-old broiler chickens (n = 240) were randomized into four groups: saline-challenged broiler chickens fed a basal diet (Con), LPS-challenged broiler chickens on a basal diet (LPS), and LPS-treated broiler chickens on a basal diet containing either 200 or 500 mg/kg of quercetin (Que200+LPS or Que500+LPS). Quercetin (200 mg/kg) significantly alleviated LPS-induced decreased duodenal, jejunal, and illeal villus height and increased the crypt depth in these regions. Quercetin significantly inhibited LPS-induced jejunal oxidative stress, including downregulated reactive oxygen species (ROS), malondialdehyde (MDA), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels, and it upregulated superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels. Quercetin relieved LPS-induced jejunal mitochondria damage and upregulated mitochondrial DNA copy number-related gene expression, including cytochrome c oxidase subunit 1 (COX1), ATP synthase F0 subunit 6 (ATP6), and NADH dehydrogenase subunit 1 (ND1). Quercetin attenuated the LPS-induced inhibition of Nrf2 activation, translocation, and downstream gene expression, including heme oxygenase-1 (HO-1), NAD (P) H dehydrogenase quinone 1 (NQO1), and manganese superoxide dismutase (SOD2). Additionally, quercetin attenuated the LPS-inhibition of c-Jun N-terminal kinase (JNK), Extracellular Regulated protein Kinases (ERK), and p38MAPK (p38) phosphorylation in the MAPK pathway. Thus, quercetin attenuated LPS-induced oxidative stress in the intestines of broiler chickens via the MAPK/Nrf2 signaling pathway.

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“…However, MGC803/DDP cells showed significant resistance to cisplatin. Bax, cleaved-caspase-3 and cleaved-PARP were regarded as factors of regulating cell apoptosis [24]. Our experimental results showed that the above protein levels were markedly upregulated by cisplatin in MGC-803 and MGC-803/ DDP cells.…”

Section: Discussionmentioning

confidence: 67%

Lidocaine alleviates cisplatin resistance and inhibits migration of MGC-803/DDP cells through decreasing miR-10b

Zhang

et al. 2020

Cell Cycle

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Although chemotherapy is one of the effective means of treating gastric cancer, the resistance of chemotherapeutic drugs has followed. And the mechanisms of resistance are not completely clear. The main aim of this article was to develop a kind of drug that could reduce the resistance of cisplatin on gastric cancer cells.The MGC-803 and MGC-803/DDP cells were treated by cisplatin for 48 h and Lidocaine (Lido) for 24 h. Cell viability, apoptosis, migration and invasion were tested by cell counting kit-8 (CCK-8) assay, apoptosis assay, western blot, migration and invasion assay. After MGC-803/DDP cells were transfected for 48 h, the expression of microRNA-10b (miR-10b) were detected by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). Activation of AKT/mTOR and β-catenin pathways was tested by western blot.Cisplatin caused MGC-803 and MGC-803/DDP cell apoptosis, and MGC-803/DDP cells possessed higher cisplatin resistance than MGC-803 cells. Lido reduced the cisplatin resistance of MGC-803/DDP cells. Besides, Lido inhibited MGC-803/DDP cell migration and invasion. In addition, Lido declined cisplatin resistance by down-regulating miR-10b. Lido also repressed AKT/mTOR and β-catenin pathway by down-regulating miR-10b. This article explained the role of Lido in cisplatin resistance in MGC-803/DDP cells. Furthermore, Lido weakened the cisplatin resistance in MGC-803/DDP cells at least in part through decreasing the expression of miR-10b.

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Quercetin protected against isoniazide‐induced HepG2 cell apoptosis by activating the SIRT1/ERK pathway

Cited by 28 publications

References 36 publications

Curcumin attenuates isoniazid‐induced hepatotoxicity by upregulating the SIRT1/PGC‐1α/NRF1 pathway

Curcumin attenuates isoniazid‐induced hepatotoxicity by upregulating the SIRT1/PGC‐1α/NRF1 pathway

Quercetin Protects against Lipopolysaccharide-Induced Intestinal Oxidative Stress in Broiler Chickens through Activation of Nrf2 Pathway

Lidocaine alleviates cisplatin resistance and inhibits migration of MGC-803/DDP cells through decreasing miR-10b

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