Curcumin reduces the risk of chronic kidney damage in mice with nonalcoholic steatohepatitis by modulating endoplasmic reticulum stress and MAPK signaling

Afrin, Mst. Rejina; Arumugam, Somasundaram; Rahman, Azizur; Karuppagounder, Vengadeshprabhu; Harima, Meilei; Sano, Hiroshi; Miyashita, Shizuka; Suzuki, Kenji; Ueno, K.; Yoneyama, Hiroyuki; Watanabe, Kenichi

doi:10.1016/j.intimp.2017.05.035

Cited by 31 publications

(13 citation statements)

References 35 publications

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“…Recent studies found that the MAPK family members (JNK, p38, and ERK) and AP-1 (c-Fos and c-Jun) are well known to be essential to osteoclast formation and proinflammation [ 46 , 47 ]. The p-JNK may be related to chronic kidney damage and immunotoxicity [ 48 , 49 ]. On the other hand, NF- κ B and JNK are bound up with ROS [ 50 , 51 ].…”

Section: Discussionmentioning

confidence: 99%

Dicalcium Silicate Induced Proinflammatory Responses through TLR2-Mediated NF-κB and JNK Pathways in the Murine RAW 264.7 Macrophage Cell Line

Lai

Chen

Cao

et al. 2018

Mediators of Inflammation

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Proinflammatory responses are important aspects of the immune response to biomaterials, which may cause peri-implantitis and implant shedding. The purpose of this study was to test the cytotoxicity and proinflammatory effects of dicalcium silicate particles on RAW 264.7 macrophages and to investigate the proinflammatory response mechanism induced by C2S and tricalcium phosphate (TCP). C2S and TCP particles were characterized using scanning electron microscopy (SEM), energy spectrum analysis (EDS) and X-ray diffraction (XRD). Cytotoxicity and apoptosis assays with C2S and TCP in the murine RAW 264.7 cell line were tested using the cell counting kit-8 (CCK-8) assay and flow cytometry (FCM). The detection results showed that C2S and TCP particles had no obvious toxicity in RAW 264.7 cells and did not cause obvious apoptosis, although they both caused an oxidative stress response by producing ROS when the concentrations were at 100 μg/mL. C2S particles are likely to induce a proinflammatory response by inducing high TLR2, TNF-α mRNA, TNF-α proinflammatory cytokine, p-IκB, and p-JNK1 + JNK2 + JNK3 expression levels. When we added siRNA-TLR2-1, a significant reduction was observed. These findings support the theory that C2S particles induce proinflammatory responses through the TLR2-mediated NF-κB and JNK pathways in the murine RAW 264.7 macrophage cell line.

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Section: Discussionmentioning

confidence: 99%

Dicalcium Silicate Induced Proinflammatory Responses through TLR2-Mediated NF-κB and JNK Pathways in the Murine RAW 264.7 Macrophage Cell Line

Lai

Chen

Cao

et al. 2018

Mediators of Inflammation

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“…Streptozotocin (STZ) is used to induce type 1 diabetes with the toxicity to pancreatic β cells. When mice administered with STZ were fed with HFD, they developed NASH with oxidative stress ( 24 , 44 ). In the STAM model, low-dose STZ (200 μg) is administered to neonatal mice via a single subcutaneous injection immediately after birth, followed by feeding HFD (32% fat) at 4 weeks of age ( 25 ).…”

Section: Murine Nash Models and Their Characteristicsmentioning

confidence: 99%

Roles of Hepatic Innate and Innate-Like Lymphocytes in Nonalcoholic Steatohepatitis

Chen

Tian

2020

Front. Immunol.

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Nonalcoholic steatohepatitis (NASH), a progressive form of nonalcoholic fatty liver disease (NAFLD), is accompanied by steatosis, hepatocyte injury and liver inflammation, which has been a health problem in the world as one of the major high risk factors of cirrhosis and hepatocellular carcinoma (HCC). Complex immune responses involving T cells, B cells, Kupffer cells, monocytes, neutrophils, DCs and other innate lymphocytes account for the pathogenesis of NASH; however, the underlying mechanisms have not been clearly elucidated in detail. In the liver, innate and innate-like lymphocytes account for more than two-thirds of total lymphocytes and play an important role in maintaining the immune homeostasis. Therefore, their roles in the progression of NASH deserves investigation. In this review, we summarized murine NASH models for immunological studies, including the diet-induced NASH, chemical-induced NASH and genetic-induced NASH. The role of innate and innate-like lymphocytes including NK cells, ILCs, NKT, γδT and MAIT cells in the progression of NASH were elucidated. Further, the metabolic regulation of the innate immune response was addressed in consideration to explain the molecular mechanisms. Based on the findings of the reviewed studies, strategies of immune intervention are proposed to control the progression of NASH.

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“…Each group was separated into two subgroups for treatment with either curcumin at a dose of 100 mg/kg per d (Sigma Chemicals Co. Purity (HPLC) > 80 %) suspended in 5 % carboxymethyl cellulose (CMC) (22)(23)(24)(25)(26) or the same volume/weight of the 5 % CMC vehicle by oral gavage once a day from the day after surgery for 28 d. BDL procedure was accomplished as described previously (27) . Concisely, under general anaesthesia by xylazine (10 mg/kg) and ketamine (90 mg/kg) intraperitoneally, the common bile duct was exposed by a midline abdominal incision under sterile conditions.…”

Section: Animals and Experimental Proceduresmentioning

confidence: 99%

Curcumin attenuates hepatic fibrosis and insulin resistance induced by bile duct ligation in rats

et al. 2018

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Recent studies have strongly indicated the hepatoprotective effect of curcumin; however, the precise mechanisms are not well understood. This study aimed to determine the protective effect of curcumin on hepatic damage and hepatic insulin resistance in biliary duct ligated (BDL) fibrotic rat model. To accomplish this, male Wistar rats were divided into four groups (eight for each): sham group, BDL group, sham+Cur group and BDL+Cur group. The last two groups received curcumin at a dose of 100 mg/kg daily for 4 weeks. The mRNA/protein expression levels of Ras-related C3 botulinum toxin substrate 1 (Rac1), Rac1-GTP, dinucleotide phosphate oxidase 1 (NOX1), signal transducer and activator of transcription 3 (STAT3), suppressor of cytokine signalling 3 (SOCS3), insulin receptor substrate 1 (IRS1), extracellular signal-regulated kinase 1 (ERK1), specific protein 1 (Sp1) and hypoxia-inducible factor-1α (HIF-1α) were measured by real-time PCR and Western blotting, respectively. Fasting blood glucose, insulin and Leptin levels were determined and homoeostasis model assessment-estimated insulin resistance, as an index of insulin resistance, was calculated. Curcumin significantly attenuated liver injury and fibrosis, including amelioration of liver histological changes, reduction of hepatic enzymes, as well as decreased expression of liver fibrogenesis-associated variables, including Rac1, Rac1-GTP, NOX1, ERK1, HIF-1α and Sp1. Curcumin also attenuated leptin level and insulin resistance, which had increased in BDL rats (P<0·05). Furthermore, compared with the BDL group, we observed an increase in IRS1 and a decrease in SOCS3 and STAT3 expression in the curcumin-treated BDL group (P<0·05), indicating return of these parameters towards normalcy. In conclusion, Curcumin showed hepatoprotective activity against BDL-induced liver injury and hepatic insulin resistance by influencing the expression of some genes/proteins involved in these processes, and the results suggest that it can be used as a therapeutic option.

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Curcumin reduces the risk of chronic kidney damage in mice with nonalcoholic steatohepatitis by modulating endoplasmic reticulum stress and MAPK signaling

Cited by 31 publications

References 35 publications

Dicalcium Silicate Induced Proinflammatory Responses through TLR2-Mediated NF-κB and JNK Pathways in the Murine RAW 264.7 Macrophage Cell Line

Dicalcium Silicate Induced Proinflammatory Responses through TLR2-Mediated NF-κB and JNK Pathways in the Murine RAW 264.7 Macrophage Cell Line

Roles of Hepatic Innate and Innate-Like Lymphocytes in Nonalcoholic Steatohepatitis

Curcumin attenuates hepatic fibrosis and insulin resistance induced by bile duct ligation in rats

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