One of the key mechanisms alcoholic liver disease is oxidative stress. Both Curcumin and Baicalin exert antioxidant effects, but mechanism their combined effects ethanol-induced injury still unclear. This study was conducted to evaluate dual activity with against in rats. Rats were divided into five groups, a control, ethanol, ethanol + (50 mg/kg), +Baicalin group ten rats per group. The on enzymes, stress indicators levels Nrf2/HO-1 pathway related proteins mRNA observed along...

Abstract Nickel oxide nanoparticles (Nano NiO) bears hepatotoxicity, while whether it leads to liver fibrosis remains unclear. The aim of this study was establish the Nano NiO‐induced hepatic model in vivo and investigate roles transforming growth factor β1 (TGF‐β1) Smad pathway activation, epithelial‐mesenchymal transition (EMT) occurrence, extracellular matrix (ECM) deposition vitro. Male Wistar rats were exposed 0.015, 0.06, 0.24 mg/kg NiO by intratracheal instilling twice a week for 9...

The aim of the present study was to explore role oxidative stress in liver toxicity induced by nickel oxide nanoparticles (nano‑NiO) rats. Male Wistar rats received saline (control), nano‑NiO [0.015, 0.06 or 0.24 mg/kg body weight (b.w.)] micro‑NiO (0.24 b.w.) intratracheal instilling twice a week for 6 weeks. Liver tissues were then collected and examined biomarkers nitrative stress, as well mRNA expression heme oxygenase (HO)‑1 metallothionein (MT)‑1. results demonstrated that NiO exposure...

Nickel can induce apoptosis of testicular Leydig cells in mice, whereas the mechanisms remain unclear. In this study, we investigated role nickel-induced reactive oxygen species (ROS) generation mitochondria and endoplasmic reticulum stress (ERS) mediated pathways rat cells. Fluorescent DCF Annexin-V FITC/PI staining were performed to measure production ROS RT-qPCR Western blot conducted analyze key genes proteins involved ERS apoptotic pathways. The results showed that nickel sulfate...

Fatty acid (FA) biosynthesis is a crucial cellular process that converts nutrients into metabolic intermediates necessary for membrane biosynthesis, energy storage, and the production of signaling molecules. Acetyl-CoA carboxylase (ACACA) plays pivotal catalytic role in both fatty synthesis oxidation. This cytosolic enzyme catalyzes carboxylation acetyl-CoA to malonyl-CoA, which represents first rate-limiting step de novo biosynthesis. In this study, we developed rapid effective purification...

Nickel oxide nanoparticles (NiONPs) can induce liver fibrosis, and their mechanism may be related to non-coding RNA, nuclear receptor signal transduction ferroptosis, but the regulatory relationship between them is not clear. In this study, we aimed investigate role of hsa_circ_0001944 in regulating Farnesol X (FXR)/Toll-like 4 (TLR4) pathway ferroptosis NiONPs-induced collagen deposition. We observed decreased FXR expression, increased TLR4 expression alterations features both rat fibrosis...

This study determined whether nickel sulfate (Ni)-induced reproductive damage occurs via apoptosis and oxidative stress to examine the expression of Bax c-kit their effects on Ni exposure. The also explored protective grape seed proanthocyanidin extract (GSPE) against toxicity in testes. Wistar rats were treated with normal saline, alone (1.25, 2.5, 5 mg/kg/day), (2.5 mg/kg/day) plus GSPE (50 100 mg/kg/day). After 30 days, significantly decreased sperm motility percentage S-phase cells...

This study aimed to explore the role of NF-κB signaling pathway in rat liver toxicity after nano NiO exposure.

Cisplatin (CIS) is widely applied for its antihematological malignancies properties and as antisolid tumors drugs. However, it could cause testicular damage related with oxidative stress testosterone synthesis disorder. Studies reported that grape seed procyanidins extract (GSPE) improve CIS induced-testes lesion via scavenging free radicals in animals, although mechanisms were unclear. Therefore, the purpose of present study was to explore antagonistic GSPE on CIS-induced testes lesion....

Abstract Nickel oxide nanoparticles (NiO NPs) causes pulmonary fibrosis via activating transforming growth factor‐β1 (TGF‐β1) in rats, but its upstream regulatory mechanisms are unknown. This study aimed to explore the role of long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) NiO NPs‐induced collagen deposition. Male Wistar rats were intratracheally instilled with NPs (0.015, 0.06, and 0.24 mg/kg b.w.) twice a week for 9 weeks. Human lung adenocarcinoma epithelial cells (A549...

Nickel oxide nanoparticles (nano NiO) could induce hepatocyte apoptosis, while its potential mechanisms are unclear. This study aimed to explore the role of endoplasmic reticulum (ER) stress pathways in apoptosis induced by nano NiO. Male Wistar rats were administrated with NiO (0.015, 0.06, and 0.24 mg/kg b.w.) micro (0.24 intratracheal instillation twice a week for 6 weeks. We measured levels TdT-mediated dUTP nick-end labeling (TUNEL) staining, ER related gene protein expression rat...

ABSTRACT With the progress of nanotechnology, nano nickel oxide (NiO) has been extensively used as sensors, battery electrodes, catalysts, and cosmetics. Previous researches verified that NiO could exert pulmonary toxicity, but its mechanism was unclear. To shed light upon this, role nuclear factor‐ κ B (NF‐ B) activation Th1/Th2 imbalance were to explore in damage induced by NiO. Male Wistar rats randomized into control group, groups (0.015, 0.06, 0.24 mg kg −1 ) micro group (0.024 treated...

Nickel oxide nanoparticles (NiONPs) are toxic heavy metal compounds that induce liver fibrosis and metabolic disorders. Current research shows the intestinal microbiota regulates metabolism through gut-liver axis. However, it is unclear whether NiONPs affect relationship between Therefore, in this study, we established model by administering 0.015, 0.06 0.24 mg/mL tracheal instillation twice a week for 9 weeks rats, then collected serum fecal sample whole metabolomics metagenomic sequencing....

Long noncoding RNA maternally expressed gene 3 (lncRNA MEG3) was down-regulated in pulmonary fibrosis of rats induced by Nickel oxide nanoparticles (NiO NPs), while the downstream regulatory mechanisms MEG3 remain unclear. This study aimed to investigate relationship among MEG3, Hedgehog (Hh) signaling pathway and autophagy caused NiO NPs. The model constructed intratracheal instillation 0.015, 0.06, 0.24 mg/kg NPs twice a week for 9 weeks. Collagen deposition established treating A549 cells...

With the widespread use of manganese dioxide nanoparticles (nano MnO 2 ), health hazards have also emerged. The inflammatory damage brain tissues could result from nano , in which underlying mechanism is still unclear. During this study, we aimed to investigate role ROS-mediated p38 MAPK pathway -induced response BV2 microglial cells. injury model was established by treating cells with 2.5, 5.0, and 10.0 μg/mL suspensions for 12 h. Then, reactive oxygen species (ROS) scavenger (20 nM...

The aim of present study was to investigate the subchronic pulmonary toxicity induced by nano nickel oxide (NiO) and its potential mechanism in rats. Male Wistar rats received intratracheally instilled NiO (0.015, 0.06 0.24 mg/kg b. w), micro (0.24 w) normal saline (control) twice a week for 6 weeks. Serum lung tissue were collected quantify biomarkers inflammatory response oxidative stress as well HO-1 MT-1 mRNA expression. general assessed through slow increase body weight decreased food...

Nickel oxide nanoparticles (Nano NiO) could induce pulmonary fibrosis, however, the mechanisms are still unknown. The aim of present study was to explore roles transforming growth factor-β1 (TGF-β1), mitogen-activated protein kinase (MAPK) pathway and MMPs/TIMPs balance in Nano NiO-induced fibrosis. For that purpose, we first established human lung adenocarcinoma epithelial cells (A549 cells) model collagen excessive formation through detecting levels hydroxyproline (Hyp) type I (Col-I)....

Abstract Our previous study demonstrated that nano nickel oxide (NiO) induce pulmonary fibrosis in rats and collagen excessive formation A549 cells, which mechanism was related with the increasing transforming growth factor β1 (TGF‐β1) secretion. However, it remains unclear understanding role of TGF‐β1 formation. Here, we found NiO could directly promote epithelial‐mesenchymal transition (EMT) via TGF‐β1/Smads pathway cells. First, cytotoxicity induced by has a dose‐ time‐dependent manner...

The lung inflammatory damage could result from the nickel oxide nanoparticles (NiO NPs), in which underlying mechanism is still unclear. This article explored roles of long noncoding RNA maternally expressed gene 3 (lncRNA MEG3) and p38 mitogen activated protein kinases (p38 MAPK) pathway pulmonary injury induced by NiO NPs. Wistar rats were treated with NPs suspensions (0.015, 0.06, 0.24 mg/kg) intratracheal instillation twice-weekly for 9 weeks. Meanwhile, A549 cells (25, 50, 100 μg/ml) 24...

Long noncoding RNA maternally expressed gene 3 (MEG3) involves in fibrotic diseases, but its role nickel oxide nanoparticles (NiO NPs)-induced pulmonary fibrosis remains unclear. The present study aimed to explore the relationships among MEG3, transforming growth factor-β1 (TGF-β1) and phosphoinositide 3-kinase (PI3K)/AKT pathway NiO NPs-induced fibrosis. Wistar rats were intratracheally instilled with NPs twice a week for 9 weeks, human lung adenocarcinoma epithelial cells (A549 cells)...

Cisplatin (CP) is one of important tumour chemotherapeutic agents in humans. Previous reports claim that CP can cause testicular toxicity. The aim this study was to evaluate the potential effects testes rats. Male Wistar rats were intraperitoneally administered at 1.0, 2.5, and 5.0 mg/kg for three consecutive days. After exposure, significantly inhibited activities succinate dehydrogenase (SDH) malate (MDH), but it elevated acid phosphatase (ACP), alkaline (AKP), lactate (LDH) group....

Testicular toxicity is an adverse reaction of the effective chemotherapy drug cisplatin (CIS). Our previous study found that grape seed proanthocyanidin extract (GSPE) had a protective effect on CIS-induced testicular toxicity. However, mechanism GSPE against remains unknown. In this study, we aimed to investigate whether can reduce and its potential in rats. The results showed ameliorated apoptosis cells inhibited protein levels Bad, Cyt c, caspase-9, caspase-3, caspase-12, GRP78, CHOP,...

Abstract Nickel oxide nanoparticles (Nano NiO) lead to pulmonary fibrosis, and the mechanisms are associated with epigenetics. This study aimed clarify regulatory relationship among long noncoding RNA HOXA transcript antisense myeloid-specific 1 (HOTAIRM1), DNA methylation expression of protein kinase C beta (PRKCB), JNK/c-Jun pathway in Nano NiO-induced fibrosis. Therefore, we constructed rat fibrosis model by intratracheal instillation NiO twice a week for 9 weeks established collagen...