SIRT1 alleviates isoniazid-induced hepatocyte injury by reducing histone acetylation in the IL-6 promoter region

Zhang, Yiyang; Li, Yingshu; Li, Jinfeng; Li, Biao; Chong, Yingzhi; Zheng, Gen; Sun, Shiqun; Fang, Feng

doi:10.1016/j.intimp.2018.11.054

Cited by 24 publications

(17 citation statements)

References 34 publications

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“…Previous studies have investigated non-specific factors causing ADLI, such as interleukin (IL) and tumour necrosis factor (TNF). 2,[17][18][19] However, the underlying mechanism of drug-induced liver injury Clinical qualification of biomarkers requires good accuracy, reproducibility, and applicability. The closed loop structure of cir-cRNA makes it highly conserved and remarkably stable, and thus, it is not degraded by exonucleases.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have also identified the role of histone modifications in ADLI progression. 2,3 And a study implicated enhancer of zest 1 (EZH1) and EZH2 are responsible for (tri-/di-) methylation on histone 3 lysine 27 (H3K27me2/3) in liver regeneration. 33 According to Bae et al, combined loss of EZH1 and EZH2 in hepatocytes of mice was associated with spontaneous liver damage.…”

Section: Discussionmentioning

confidence: 99%

“…Drug‐induced liver injury is a significant obstacle in the treatment of TB. Previous studies have investigated non‐specific factors causing ADLI, such as interleukin (IL) and tumour necrosis factor (TNF) 2,17–19 . However, the underlying mechanism of drug‐induced liver injury with anti‐TB drugs needs further exploration to develop novel therapeutic targets.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have reported that methylation, acetylation, and non‐coding RNAs in epigenesis are closely related to ADLI. However, further studies on the role of circRNAs in ADLI are needed 2–5 …”

Section: Introductionmentioning

confidence: 99%

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Screening differential circular RNA expression profiles reveals the regulatory role of circMARS in anti‐tuberculosis drug‐induced liver injury

Ren

et al. 2022

J Cellular Molecular Medi

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Tuberculosis (TB) is a chronic infectious disease caused byMycobacterium tuberculosis. It is a preventable and treatable disease mainly transmitted from person to person through the air. Globally, China has a high burden of TB and the third-highest incidence behind India and Indonesia. According to the global tuberculosis report (2019) by the World Health Organization (WHO), there were about 866,000 TB cases and 40,000 TB deaths in China. 1 One of the health-related goals of sustainable development is to curb the TB epidemic by 2030. The World Health Assembly passed the resolution with ambitious targets, but it is not an easy promise. Standardized chemotherapy is a crucial means to achieve this goal. However, the adverse effects of chemotherapeutic drugs such as anti-tuberculosis

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Screening differential circular RNA expression profiles reveals the regulatory role of circMARS in anti‐tuberculosis drug‐induced liver injury

Ren

et al. 2022

J Cellular Molecular Medi

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“…In addition to the binding of transcription factors to the IL-6 promoter, chromatin structure also plays a key role in regulating gene expression (21,22). Histone acetylation, which is catalyzed by histone acetyltransferases (HATs) and is one determinant of transcription efficiency, is associated with an enhancement of access of transcription factors, leading ultimately to a more active state partly due to a weakened interaction between histone proteins and DNA strands (23,24).…”

Section: Introductionmentioning

confidence: 99%

Modulation of IL-6 Expression by KLF4-Mediated Transactivation and PCAF-Mediated Acetylation in Sublytic C5b-9-Induced Rat Glomerular Mesangial Cells

Zhang

et al. 2022

Front. Immunol.

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Interleukin-6 (IL-6) overproduction has been considered to contribute to inflammatory damage of glomerular mesangial cells (GMCs) in human mesangial proliferative glomerulonephritis (MsPGN) and its rat model called Thy-1 nephritis (Thy-1N). However, the regulatory mechanisms of IL-6 expression in GMCs upon sublytic C5b-9 timulation remain poorly understood. We found that Krüppel-like factor 4 (KLF4) bound to the IL-6 promoter (−618 to −126 nt) and activated IL-6 gene transcription. Furthermore, lysine residue 224 of KLF4 was acetylated by p300/CBP-associated factor (PCAF), which was important for KLF4-mediated transactivation. Moreover, lysine residue 5 on histone H2B and lysine residue 9 on histone H3 at the IL-6 promoter were also acetylated by PCAF, which resulted in an increase in IL-6 transcription. Besides, NF-κB activation promoted IL-6 expression by elevating the expression of PCAF. Overall, these findings suggest that sublytic C5b-9-induced the expression of IL-6 involves KLF4-mediated transactivation, PCAF-mediated acetylation of KLF4 and histones, and NF-κB activation in GMCs.

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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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SIRT1 alleviates isoniazid-induced hepatocyte injury by reducing histone acetylation in the IL-6 promoter region

Cited by 24 publications

References 34 publications

Screening differential circular RNA expression profiles reveals the regulatory role of circMARS in anti‐tuberculosis drug‐induced liver injury

Screening differential circular RNA expression profiles reveals the regulatory role of circMARS in anti‐tuberculosis drug‐induced liver injury

Modulation of IL-6 Expression by KLF4-Mediated Transactivation and PCAF-Mediated Acetylation in Sublytic C5b-9-Induced Rat Glomerular Mesangial Cells

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

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