Piperlongumine attenuates bile duct ligation-induced liver fibrosis in mice via inhibition of TGF-β1/Smad and EMT pathways

Chilvery, Shrilekha; Bansod, Sapana; Saifi, Mohd Aslam; Godugu, Chandraiah

doi:10.1016/j.intimp.2020.106909

Cited by 26 publications

(14 citation statements)

References 47 publications

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“…However, when there is chronic liver injury, chronic inflammation and fibrosis lead to pathological conditions [29,95]. HSCs play an important role in fibrosis process, which can be activated by IL-6, transforming growth factor-β (TGF-β), and platelet-derived growth factor [96][97][98]. After liver injury, KCs not only produce pro-inflammatory factors to activate HSCs but also recruit CCR2+/Ly-6Chi monocytes into injured liver to sustain activation of HSCs [99].…”

Section: Roles Of Trem In Hepatic Fibrosismentioning

confidence: 99%

Function of TREM1 and TREM2 in Liver-Related Diseases

Sun

Feng

Tang

2020

Cells

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TREM1 and TREM2 are members of the triggering receptors expressed on myeloid cells (TREM) family. Both TREM1 and TREM2 are immunoglobulin superfamily receptors. Their main function is to identify foreign antigens and toxic substances, thereby adjusting the inflammatory response. In the liver, TREM1 and TREM2 are expressed on non-parenchymal cells, such as liver sinusoidal endothelial cells, Kupffer cells, and hepatic stellate cells, and cells which infiltrate the liver in response to injury including monocyte-derived macrophages and neutrophils. The function of TREM1 and TREM2 in inflammatory response depends on Toll-like receptor 4. TREM1 mainly augments inflammation during acute inflammation, while TREM2 mainly inhibits chronic inflammation to protect the liver from pathological changes. Chronic inflammation often induces metabolic abnormalities, fibrosis, and tumorigenesis. The above physiological changes lead to liver-related diseases, such as liver injury, nonalcoholic steatohepatitis, hepatic fibrosis, and hepatocellular carcinoma. Here, we review the function of TREM1 and TREM2 in different liver diseases based on inflammation, providing a more comprehensive perspective for the treatment of liver-related diseases.

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Section: Roles Of Trem In Hepatic Fibrosismentioning

confidence: 99%

Function of TREM1 and TREM2 in Liver-Related Diseases

Sun

Feng

Tang

2020

Cells

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“…The HRP-conjugated secondary antibodies were added and sections were stained with 3, 3-diaminobenzidine (DAB) reagent. Further, sections were counterstained with hematoxylin and images were observed using a light microscope (CX21i Olympus, India) 26 . Quantitative analysis of fibrotic and immunopositive area were analyzed using ImageJ software (NIH, USA).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of discoidin domain receptors by imatinib prevented pancreatic fibrosis demonstrated in experimental chronic pancreatitis model

Bansod

Saifi

Godugu

2021

Sci Rep

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Discoidin domain receptors (DDR1 and DDR2) are the collagen receptors of the family tyrosine kinases, which play significant role in the diseases like inflammation, fibrosis and cancer. Chronic pancreatitis (CP) is a fibro-inflammatory disease in which recurrent pancreatic inflammation leads to pancreatic fibrosis. In the present study, we have investigated the role of DDR1 and DDR2 in CP. The induced expression of DDR1 and DDR2 was observed in primary pancreatic stellate cells (PSCs) and cerulein-induced CP. Subsequently, the protective effects of DDR1/DDR2 inhibitor, imatinib (IMT) were investigated. Pharmacological intervention with IMT effectively downregulated DDR1 and DDR2 expression. Further, IMT treatment reduced pancreatic injury, inflammation, extracellular matrix deposition and PSCs activation along with inhibition of TGF-β1/Smad signaling pathway. Taken together, these results suggest that inhibition of DDR1 and DDR2 controls pancreatic inflammation and fibrosis, which could represent an attractive and promising therapeutic strategy for the treatment of CP.

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“…Then, supernatant was collected and protein concentrations were estimated by Bicinchoninic acid assay. An equal amount of protein were run on 10% sodium dodecyl sulfate polyacrylamide gel electrophoresis and transferred to a nitrocellulose membrane following the standard protocol 28,31 . The primary antibodies, such as NFκB p65 (Catalogue no.‐D14E12, #8242) and p‐NFκB p65 (Catalogue no.‐93H1, #3033) were procured from Cell Signaling Technology, USA, whereas iNOS (Catalogue no.‐N9657) were purchased from Sigma–Aldrich, USA.…”

Section: Methodsmentioning

confidence: 99%

“…An equal amount of protein were run on 10% sodium dodecyl sulfate polyacrylamide gel electrophoresis and transferred to a nitrocellulose membrane following the standard protocol. 28,31 The primary antibodies, . Densitometric analysis was performed using the ImageJ software (NIH, USA).…”

Section: Western Blot Analysismentioning

confidence: 99%

Borneol protects against cerulein‐induced oxidative stress and inflammation in acute pancreatitis mice model

Bansod

Chilvery

Saifi

et al. 2020

Environmental Toxicology

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Borneol is a commonly used flavouring substance in traditional Chinese medicine, which possesses several pharmacological activities including analgesic, antiinflammatory, and antioxidant properties. The aim of this study was to investigate the effects of borneol on cerulein‐induced acute pancreatitis (AP) model. Swiss albino mice were pretreated with borneol (100 and 300 mg/kg) daily for 7 days, before six consecutive injections of cerulein (50 μg/kg/hr, intraperitoneally). The protective effect of borneol was studied by biochemical, enzyme linked immunosorbent assay, histological, immunoblotting, and immunohistochemical analysis. Oral administration of borneol significantly attenuated pancreatic damage by reducing amylase, lipase levels and histological changes. Borneol attenuated cerulein‐induced oxidative‐nitrosative stress by decreasing malondialdehyde, nitrite levels, and elevating reduced glutathione levels. Pancreatic inflammation was ameliorated by inhibiting myeloperoxidase activity and pro‐inflammatory cytokine (Interleukins and TNF‐α) levels. Furthermore, borneol administration significantly increased nuclear factor E2‐related factor 2 (Nrf2), superoxide dismutase (SOD1) expression and reduced phospho‐NF‐κB p65 expression. Treatment with borneol significantly inhibited TNF‐α, IL‐1β, IL‐6, and inducible nitric oxide synthase expression in cerulein‐induced AP mouse model. Together, these results indicate that borneol which is currently used as US‐FDA approved food adjuvant has the potential to attenuate cerulein‐induced AP possibly by reducing the oxidative damage and pancreatic inflammation by modulating Nrf2/NF‐κB pathway.

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Piperlongumine attenuates bile duct ligation-induced liver fibrosis in mice via inhibition of TGF-β1/Smad and EMT pathways

Cited by 26 publications

References 47 publications

Function of TREM1 and TREM2 in Liver-Related Diseases

Function of TREM1 and TREM2 in Liver-Related Diseases

Inhibition of discoidin domain receptors by imatinib prevented pancreatic fibrosis demonstrated in experimental chronic pancreatitis model

Borneol protects against cerulein‐induced oxidative stress and inflammation in acute pancreatitis mice model

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