Alleviative effects from boswellic acid on acetaminophen-induced hepatic injury

Chen, Lung Che; Hu, Li; Yin, Mei

doi:10.7603/s40681-016-0009-1

Cited by 18 publications

(13 citation statements)

References 30 publications

(28 reference statements)

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“…It protected against APAP-induced hepatotoxicity in mice by improving glutathione redox, inhibiting oxidative stress and attenuating pro-inflammatory cytokines and chemokines along with histopathologic salvage. It produced restoration of glutathione reductase (GR) and heme oxygenase-1 (HO-1) activities and inhibited CYP2E1 concomitant with reduced expression of toll-like receptors; TLR-3 and -4, MyD88, NF-κBp50, NF-κB p65 and JNK in liver tissues [45].…”

Section: Introductionmentioning

confidence: 99%

Therapeutic Potential of Plants and Plant Derived Phytochemicals against Acetaminophen-Induced Liver Injury

Subramanya

Venkataraman

Meeran

et al. 2018

IJMS

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Acetaminophen (APAP), which is also known as paracetamol or N-acetyl-p-aminophenol is a safe and potent drug for fever, pain and inflammation when used at its normal therapeutic doses. It is available as over-the-counter drug and used by all the age groups. The overdose results in acute liver failure that often requires liver transplantation. Current clinical therapy for APAP-induced liver toxicity is the administration of N-acetyl-cysteine (NAC), a sulphydryl compound an approved drug which acts by replenishing cellular glutathione (GSH) stores in the liver. Over the past five decades, several studies indicate that the safety and efficacy of herbal extracts or plant derived compounds that are used either as monotherapy or as an adjunct therapy along with conventional medicines for hepatotoxicity have shown favorable responses. Phytochemicals mitigate necrotic cell death and protect against APAP-induced liver toxicityby restoring cellular antioxidant defense system, limiting oxidative stress and subsequently protecting mitochondrial dysfunction and inflammation. Recent experimental evidences indicat that these phytochemicals also regulate differential gene expression to modulate various cellular pathways that are implicated in cellular protection. Therefore, in this review, we highlight the role of the phytochemicals, which are shown to be efficacious in clinically relevant APAP-induced hepatotoxicity experimental models. In this review, we have made comprehensive attempt to delineate the molecular mechanism and the cellular targets that are modulated by the phytochemicals to mediate the cytoprotective effect against APAP-induced hepatotoxicity. In this review, we have also defined the challenges and scope of phytochemicals to be developed as drugs to target APAP-induced hepatotoxicity.

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Section: Introductionmentioning

confidence: 99%

Therapeutic Potential of Plants and Plant Derived Phytochemicals against Acetaminophen-Induced Liver Injury

Subramanya

Venkataraman

Meeran

et al. 2018

IJMS

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“…The role of miRNA in cancer progression has been well-investigated in the past decade (8–11). miRNAs can affect gene expression not only by suppressing protein translation but also by reducing the mRNA expression of a target gene, resulting in a correlation between the expression levels of miRNAs and their target genes (12–14).…”

Section: Introductionmentioning

confidence: 99%

YM500v3: a database for small RNA sequencing in human cancer research

Chung¹,

Chang

Chen³

et al. 2016

Nucleic Acids Res

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We previously presented the YM500 database, which contains >8000 small RNA sequencing (smRNA-seq) data sets and integrated analysis results for various cancer miRNome studies. In the updated YM500v3 database (http://ngs.ym.edu.tw/ym500/) presented herein, we not only focus on miRNAs but also on other functional small non-coding RNAs (sncRNAs), such as PIWI-interacting RNAs (piRNAs), tRNA-derived fragments (tRFs), small nuclear RNAs (snRNAs) and small nucleolar RNAs (snoRNAs). There is growing knowledge of the role of sncRNAs in gene regulation and tumorigenesis. We have also incorporated >10 000 cancer-related RNA-seq and >3000 more smRNA-seq data sets into the YM500v3 database. Furthermore, there are two main new sections, ‘Survival' and ‘Cancer', in this updated version. The ‘Survival’ section provides the survival analysis results in all cancer types or in a user-defined group of samples for a specific sncRNA. The ‘Cancer’ section provides the results of differential expression analyses, miRNA–gene interactions and cancer miRNA-related pathways. In the ‘Expression’ section, sncRNA expression profiles across cancer and sample types are newly provided. Cancer-related sncRNAs hold potential for both biotech applications and basic research.

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“…Intrinsic mitochondria apoptosis occurs in response to death stimuli, including activation of chemotherapeutic agents [ 10 ], serum starvation [ 11 ], ultraviolet radiation [ 12 ] and ROS [ 13 ]. Production of high levels of ROS is known to cause mitochondrial DNA damage, mitochondrial membrane permeabilization, and the release of cytochrome c from mitochondria, triggering caspase-dependent or caspase-independent cytosolic signaling events [ 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

BL-038, a Benzofuran Derivative, Induces Cell Apoptosis in Human Chondrosarcoma Cells through Reactive Oxygen Species/Mitochondrial Dysfunction and the Caspases Dependent Pathway

Liu¹,

Chen

et al. 2016

IJMS

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Chondrosarcoma is a highly malignant cartilage-forming bone tumor that has the capacity to invade locally and cause distant metastasis. Moreover, chondrosarcoma is intrinsically resistant to conventional chemotherapy or radiotherapy. The novel benzofuran derivative, BL-038 (2-amino-3-(2,6-dichlorophenyl)-6-(4-methoxyphenyl)benzofuran-4-yl acetate), has been evaluated for its anticancer effects in human chondrosarcoma cells. BL-038 caused cell apoptosis in two human chondrosarcoma cell lines, JJ012 and SW1353, but not in primary chondrocytes. Treatment of chondrosarcoma with BL-038 also induced reactive oxygen species (ROS) production. Furthermore, BL-038 decreased mitochondrial membrane potential (MMP) and changed mitochondrial-related apoptosis, by downregulating the anti-apoptotic activity members (Bcl-2, Bcl-xL) and upregulating pro-apoptotic members (Bax, Bak) of the B-cell lymphoma 2 (Bcl-2) family of proteins, key regulators of the apoptotic machinery in cells. These results demonstrate that in human chondrosarcoma cells, the apoptotic and cytotoxic effects of BL-038 are mediated by the intrinsic mitochondria-mediated apoptotic pathway, which in turn causes the release of cytochrome c, the activation of caspase-9 and caspase-3, and the cleavage of poly (ADP-ribose) polymerase (PARP), to elicit apoptosis response. Our results show that the benzofuran derivative BL-038 induces apoptosis in chondrosarcoma cells.

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Alleviative effects from boswellic acid on acetaminophen-induced hepatic injury

Cited by 18 publications

References 30 publications

Therapeutic Potential of Plants and Plant Derived Phytochemicals against Acetaminophen-Induced Liver Injury

Therapeutic Potential of Plants and Plant Derived Phytochemicals against Acetaminophen-Induced Liver Injury

YM500v3: a database for small RNA sequencing in human cancer research

BL-038, a Benzofuran Derivative, Induces Cell Apoptosis in Human Chondrosarcoma Cells through Reactive Oxygen Species/Mitochondrial Dysfunction and the Caspases Dependent Pathway

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