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Mechanisms of isoniazid and rifampicin-induced liver injury and the effects of natural medicinal ingredients: A review

Zhuang, Xiuping, Li, Li, Liu, Tianyi, Zhang, Rui, Yang, Peimin, Wang, Xin, Dai, Long·2022·Frontiers in Pharmacology
DOI 10.3389/fphar.2022.1037814PMC PMC9589499
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Abstract

Isoniazid (INH) and rifampicin (RFP) are the first-line medications for tuberculosis treatment, and liver injury is the major adverse effect. Natural medicinal ingredients provide distinct benefits in alleviating patients’ symptoms, lowering the liver injury risk, delaying disease progression, and strengthening the body’s ability to heal. This paper summarises the recent research on the mechanisms of INH and RFP-induced liver injury and the effects of natural medicinal ingredients. It is believed that INH-induced liver injury may be attributed to oxidative stress, mitochondrial dysfunction, drug metabolic enzymes, protoporphyrin IX accumulation, endoplasmic reticulum stress, bile transport imbalance, and immune response. RFP-induced liver injury is mainly related to cholestasis, endoplasmic reticulum stress, and liver lipid accumulation. However, the combined effect of INH and RFP on liver injury risk is still uncertain. RFP can increase INH-induced hepatotoxicity by regulating the expression of drug-metabolizing enzymes and transporters. In contrast, INH can antagonize RFP-induced liver injury by reducing the total bilirubin level in the blood. Sagittaria sagittifolia polysaccharide, quercetin, gallic acid, and other natural medicinal ingredients play protective roles on INH and RFP-induced liver injury by enhancing the body’s antioxidant capacity, regulating metabolism, inhibiting cell apoptosis, and reducing the inflammatory response. There are still many gaps in the literature on INH and RFP-induced liver injury mechanisms and the effects of natural medicinal ingredients. Thus, further research should be carried out from the perspectives of liver injury phenotype, injury markers, in vitro and in vivo liver injury model construction, and liver-gut axis. This paper comprehensively reviewed the literature on mechanisms involved in INH and RFP-induced liver injury and the status of developing new drugs against INH and RFP-induced liver injury. In addition, this review also highlighted the uses and advantages of natural medicinal ingredients in treating drug-induced liver injury.

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FIGURE 1 The mechanisms of oxidative stress injury caused by INH (Compensatory Nrf2/ARE antioxidative stress system inhibition, production of lipid peroxides, activation of NF-κB signaling pathway and the JNK/Bax pathway play important roles in INH-induced oxidative stress injury). Notes: INH, isoniazid; ROS, reactive oxygen species; MDA, malonic dialdehyde; Nrf2, nuclear erythroid 2-related factor 2; Keap1, kelch-like ECH-associated protein 1; PKCδ, protein kinase Cδ; ERK1, extracellular signal-regulated protein kinase 1; ARE, antioxidant response element; HO-1, heme oxygenase 1; GCLC, glutamine-l-cysteine ligase; NQO1, quinone oxidoreductase 1; NF-κB, nuclear factor-κB; IκB, NF-κB inhibitory protein; JNK, c-jun N-terminal kinase; ASK1, apoptosis signal-regulating kinase 1; Src, Src kinase; GSTπ, glutathione S-transferase π; MLK3, mixed-lineage protein kinase 3.
FIGURE 1 The mechanisms of oxidative stress injury caused by INH (Compensatory Nrf2/ARE antioxidative stress system inhibition, production of lipid peroxides, activation of NF-κB signaling pathway and the JNK/Bax pathway play important roles in INH-induced oxidative stress injury). Notes: INH, isoniazid; ROS, reactive oxygen species; MDA, malonic dialdehyde; Nrf2, nuclear erythroid 2-related factor 2; Keap1, kelch-like ECH-associated protein 1; PKCδ, protein kinase Cδ; ERK1, extracellular signal-regulated protein kinase 1; ARE, antioxidant response element; HO-1, heme oxygenase 1; GCLC, glutamine-l-cysteine ligase; NQO1, quinone oxidoreductase 1; NF-κB, nuclear factor-κB; IκB, NF-κB inhibitory protein; JNK, c-jun N-terminal kinase; ASK1, apoptosis signal-regulating kinase 1; Src, Src kinase; GSTπ, glutathione S-transferase π; MLK3, mixed-lineage protein kinase 3.CC BY · PubMed Central
FIGURE 2 The mechanisms of INH-induced mitochondrial dysfunction (INH contributes to mitochondrial dysfunction by stimulating the continued opening of mPTP, disrupting mitochondrial biogenesis, inducing mitochondrial dynamics imbalance, and inhibiting mitochondrial respiratory chain enzyme activity). Notes: mPTP, mitochondrion permeability transition pore; Cyt C, cytochrome C; APAF-1, apoptotic protease activating factor-1; SIRT1, silent information regulator 1; PGC1α, peroxisome proliferator-activated receptor-gamma coactivator 1α; NRF1, nuclear respiratory factor 1; mtDNA, mitochondrial DNA; Mfn2, mitofusin 2; Drp1, dynamin-related protein 1; TCA, tricarboxylic acid cycle.
FIGURE 2 The mechanisms of INH-induced mitochondrial dysfunction (INH contributes to mitochondrial dysfunction by stimulating the continued opening of mPTP, disrupting mitochondrial biogenesis, inducing mitochondrial dynamics imbalance, and inhibiting mitochondrial respiratory chain enzyme activity). Notes: mPTP, mitochondrion permeability transition pore; Cyt C, cytochrome C; APAF-1, apoptotic protease activating factor-1; SIRT1, silent information regulator 1; PGC1α, peroxisome proliferator-activated receptor-gamma coactivator 1α; NRF1, nuclear respiratory factor 1; mtDNA, mitochondrial DNA; Mfn2, mitofusin 2; Drp1, dynamin-related protein 1; TCA, tricarboxylic acid cycle.CC BY · PubMed Central
FIGURE 3 Schematic diagram of the molecular mechanisms of RFP-induced liver injury. Inhibition of FXR/SHP pathway promotes bile synthesis and activates PKC/ERK/JNK/p38 pathway to inhibit bile transport leading to cholestasis. Regulation of PERK/ATF4/CHOP and HMGB1/RAGE pathways to generate endoplasmic reticulum stress. RFP promotes hepatic fatty acid synthesis and absorption, respectively, by regulating hepatic fatty acid-related factors, resulting in the accumulation of hepatic lipids. Notes: RFP, rifampicin; FXR: farnesoid X receptor; SHP: small heterodimer partner; CYP7A1, cholesterol 7α hydroxylase; PKC, protein kinase C; ERK, extracellular signal-regulated kinases; JNK, c-jun N-terminal kinase; p38, p38 mitogen-activated protein kinases; AP-2, adaptin 2; GP78: E3 ubiquitin ligase; MRP2: multidrug resistance-associated protein 2; GRP78, glucose-regulated protein 78; HMGB1, high mobility group box 1 protein; RAGE: receptor for advanced glycation end products; PERK, protein kinase R-like endoplasmic reticulum kinase; ATF4, activating transcription factor 4; CHOP, C/EBP homologous protein; ERS, endoplasmic reticulum stress; NF-κB, nuclear factor-κB; FAS, fatty acid synthase; ACC, acetyl CoA carboxylase; SCD-1: stearoyl CoA desaturase 1; PXR: pregnane X receptor; PPAR-γ, peroxisome proliferator-activated receptor-γ; APOC3, apolipoprotein C-III, ACBP: acyl-CoA-binding protein; ThA, 3-ketoacyl-CoA thiolase A; ThB, 3-ketoacyl-CoA thiolase B; PLIN2, perilipin-2.
FIGURE 3 Schematic diagram of the molecular mechanisms of RFP-induced liver injury. Inhibition of FXR/SHP pathway promotes bile synthesis and activates PKC/ERK/JNK/p38 pathway to inhibit bile transport leading to cholestasis. Regulation of PERK/ATF4/CHOP and HMGB1/RAGE pathways to generate endoplasmic reticulum stress. RFP promotes hepatic fatty acid synthesis and absorption, respectively, by regulating hepatic fatty acid-related factors, resulting in the accumulation of hepatic lipids. Notes: RFP, rifampicin; FXR: farnesoid X receptor; SHP: small heterodimer partner; CYP7A1, cholesterol 7α hydroxylase; PKC, protein kinase C; ERK, extracellular signal-regulated kinases; JNK, c-jun N-terminal kinase; p38, p38 mitogen-activated protein kinases; AP-2, adaptin 2; GP78: E3 ubiquitin ligase; MRP2: multidrug resistance-associated protein 2; GRP78, glucose-regulated protein 78; HMGB1, high mobility group box 1 protein; RAGE: receptor for advanced glycation end products; PERK, protein kinase R-like endoplasmic reticulum kinase; ATF4, activating transcription factor 4; CHOP, C/EBP homologous protein; ERS, endoplasmic reticulum stress; NF-κB, nuclear factor-κB; FAS, fatty acid synthase; ACC, acetyl CoA carboxylase; SCD-1: stearoyl CoA desaturase 1; PXR: pregnane X receptor; PPAR-γ, peroxisome proliferator-activated receptor-γ; APOC3, apolipoprotein C-III, ACBP: acyl-CoA-binding protein; ThA, 3-ketoacyl-CoA thiolase A; ThB, 3-ketoacyl-CoA thiolase B; PLIN2, perilipin-2.CC BY · PubMed Central
FIGURE 4 Chemical structural of part monomer compounds against INH/RFP-induced liver injury. Notes: (12)-(20) identified from Crocus sativus L. extract containing polyphenols.
FIGURE 4 Chemical structural of part monomer compounds against INH/RFP-induced liver injury. Notes: (12)-(20) identified from Crocus sativus L. extract containing polyphenols.CC BY · PubMed Central
FIGURE 5 Predicted directions for later studies of INH and RFP-induced liver injury and the effects of natural medicinal ingredients. We predicted that the following six aspects might be studied in the future: Liver injury phenotype, liver injury markers, liver injury model, the liver-intestine axis, structure-activity relationship and improve efficacy, reduce toxicity.
FIGURE 5 Predicted directions for later studies of INH and RFP-induced liver injury and the effects of natural medicinal ingredients. We predicted that the following six aspects might be studied in the future: Liver injury phenotype, liver injury markers, liver injury model, the liver-intestine axis, structure-activity relationship and improve efficacy, reduce toxicity.CC BY · PubMed Central

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Cited by

Sorted by citations

Metadata

Authors
Zhuang, X., Li, L., Liu, T., Zhang, R., Yang, P., Wang, X., & Dai, L.
Venue
Frontiers in Pharmacology
Publisher
Frontiers Media SA
Published
2022-10-10
Volume
13
ISSN
1663-9812
DOI
10.3389/fphar.2022.1037814
PMC
PMC9589499
Cited by
88
References
1
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
National Natural Science Foundation of China (NO.82104506)

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