Glycyrrhizin, an HMGB1 inhibitor, Suppresses Interleukin-1β-Induced Inflammatory Responses in Chondrocytes from Patients with Osteoarthritis

Cartilage ◽  
2020 ◽  
pp. 194760352093485 ◽  
Author(s):  
Shifeng Zhou ◽  
Guodan Liu ◽  
Zhenxing Si ◽  
Luanfei Yu ◽  
Limin Hou
Keyword(s):  
Western Blot ◽  
Proinflammatory Cytokines ◽  
Inflammatory Mediators ◽  
Inflammatory Responses ◽  
High Mobility ◽  
Interleukin 1Β ◽  
Cartilage Tissue ◽  
Enzyme Linked Immunosorbent Assay ◽  
Griess Reagent ◽  
The Impact

Background High mobility group box 1 (HMGB1) is increased in osteoarthritis (OA) tissue and chondrocytes stimulated with interleukin-1β (IL-1β). Suppression of HMGB1 expression is correlated with reduced inflammatory responses induced by IL-1β. This study aimed to investigate how inhibition of HMGB1 by glycyrrhizin might affect inflammatory responses and viability of OA patient–derived chondrocytes treated with IL-1β. Design The amounts of HMGB1 in the cartilage tissue and synovial fluid in patients with OA were assessed by Western blot and enzyme-linked immunosorbent assay (ELISA). Chondrocytes were extracted from OA patients and maintained in culture. The impact of glycyrrhizin on IL-1β-induced cell toxicity and inflammatory mediators and cytokines, including prostaglandin E2 (PGE2), nitric oxide (NO), proinflammatory cytokines, and metalloproteases (MMPs), were assessed by ELISA, Western blot, quantitative real-time polymerase chain reaction, and the Griess reagent assay. Results We confirmed that HMGB1 was significantly upregulated in specimens acquired from patients with OA. HMGB1 inhibition by glycyrrhizin improved cell viability of chondrocytes treated with IL-1β. Glycyrrhizin suppressed IL-1β-induced upregulation of HMGB1 and inflammatory mediators and cytokines, including PGE2, NO, proinflammatory cytokines, and MMPs. Conclusion Our results indicate that glycyrrhizin may be a potential therapy for OA patients and these promising findings warrant further study for clinical application.

scholarly journals Heat stress combined with lipopolysaccharide alter the activity and superficial molecules of peripheral monocytes

2019 ◽  
Vol 33 ◽  
pp. 205873841982889
Author(s):  
Jiajing Luo ◽  
Yi Chen ◽  
Chengjia Ding ◽  
Jialing Qiu ◽  
Yulan Chen ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Heat Stress ◽  
Western Blot ◽  
Inflammatory Mediators ◽  
Peripheral Blood ◽  
Heat Stroke ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Rt Pcr ◽  
Tnf Α

The purpose of this study was to focus on the underlying relationship between the hyperactivity for the peripheral monocytes and heat stroke by investigating the inflammatory oxidative activity of and the expression of superficial molecules. Peripheral blood samples were collected from 10 healthy adult volunteers. Human blood monocytes were isolated by density gradient centrifugation and sequent adherent culture. The objectives were divided into four groups: 43°C heat stress combined with lipopolysaccharide (LPS) group, 43°C heat stress group, LPS group, and control group. There were 10 cases in each group. An enzyme-linked immunosorbent assay (ELISA) test was used to measure the concentrations of supernatant inflammatory mediators (tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-10 (IL-10)). After loaded by 2,7-Dichlorodi-hydrofluorescein-diacetate (DCFHDA) fluorescent probe, intracellular reactive oxygen species (ROS) levels were determined by a flow cytometry. After fluorescent microspheres incubation, the phagocytosis of monocytes was observed under a fluorescent microscope. Respectively, the flow cytometry and Western blot were used to evaluate the level of triggering receptor expressed on myeloid cells-1 (TREM-1) and Toll-like receptor-4 (TLR-4) on the monocytes. Furthermore, the mRNA expression of TREM-1 and TLR-4 was detected by real-time polymerase chain reaction (RT-PCR). The heat stress combined with LPS stimulation promoted the peripheral monocytes to produce inflammatory mediators (TNF-α, IL-1β, and IL-10) and release ROS. Otherwise, such complex strike significantly suppressed the phagocytic activity of monocytes in peripheral blood. Moreover, the expression of TREM-1, TLR-4 and CD86 was measured by the flow cytometry on peripheral monocytes which were respectively promoted by the union of heat stress and LPS. The results of Western blot and RT-PCR demonstrated the similar kinetics on these superficial molecules (TREM-1, TLR-4, and CD86) stimulated by the combination of heat stress and LPS. The underlying mechanism of the dysfunction for the peripheral monocytes may be related to the abnormal expression of superficial molecules TREM-1, TLR-4, and CD86 on the monocytes induced by heat stress and LPS.

Protective effects of quercetin on traumatic brain injury induced inflammation and oxidative stress in cortex through activating Nrf2/HO-1 pathway

2021 ◽  
Vol 39 (1) ◽  
pp. 73-84
Author(s):  
Jianqiang Song ◽  
Guoliang Du ◽  
Haiyun Wu ◽  
Xiangliang Gao ◽  
Zhen Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Western Blot ◽  
Inflammatory Responses ◽  
Enzyme Linked Immunosorbent Assay ◽  
Heme Oxygenase 1 ◽  
The Brain ◽  
And Oxidative Stress ◽  
Quercetin Treatment

Background: Traumatic brain injury (TBI) has been a serious public health issue. Clinically, there is an urgent need for agents to ameliorate the neuroinflammation and oxidative stress induced by TBI. Our previous research has demonstrated that quercetin could protect the neurological function. However, the detailed mechanism underlying this process remains poorly understood. Objective: This research was designed to investigate the mechanisms of quercetin to protect the cortical neurons. Methods: A modified weight-drop device was used for the TBI model. 5, 20 or 50 mg/kg quercetin was injected intraperitoneally to rats at 0.5, 12 and 24 h post TBI. Rats were sacrificed three days post injury and their cerebral cortex was obtained from the injured side. The rats were randomly assigned into three groups of equal number: TBI and quercetin group, TBI group, and Sham group. The brain water content was calculated to estimate the brain damage induced by TBI. Immunohistochemical and Western blot assays were utilized to investigate the neurobehavioral status. Enzyme-linked immunosorbent assay and reverse transcription polymerase chain reaction were performed to evaluate the inflammatory responses. The cortical oxidative stress was measured by estimating the activities of malondialdehyde, superoxide dismutase, catalase and glutathione-Px. Western blot was utilized to evaluate the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2) and heme oxygenase 1 (HO-1). Results: Quercetin attenuated the brain edema and microgliosis in TBI rats. Quercetin treatment attenuated cortical inflammatory responses and oxidative stress induced by TBI insults. Quercetin treatment activated the cortical Nrf2/HO-1 pathway in TBI rats. Conclusions: Quercetin ameliorated the TBI-induced neuroinflammation and oxidative stress in the cortex through activating the Nrf2/HO-1 pathway.

Fisetin Protects against Intracerebral Hemorrhage-Induced Neuroinflammation in Aged Mice

2018 ◽  
Vol 45 (3-4) ◽  
pp. 154-161 ◽  
Author(s):  
Cheng Chen ◽  
Li Yao ◽  
Jing Cui ◽  
Bao Liu
Keyword(s):  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Western Blot ◽  
Proinflammatory Cytokines ◽  
Cell Apoptosis ◽  
Calcium Binding ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Severity Scores ◽  
Cytokine Levels

Background: Fisetin is commonly used as an anti-inflammatory and neuroprotective drug. In this study, we aimed to investigate the efficacy of fisetin in alleviating intracerebral hemorrhage (ICH)-induced brain injury. Methods: Mouse ICH models were constructed using the collagenase-induction method. ICH mice received fisetin treatment at the dose of 10–90 mg/kg, followed by the evaluation of neurological deficit through neurologic severity scores (mNSS), brain water content and terminal deoxynucleotidyl transferase dUTP nick end labeling analysis of cell apoptosis. Cytokine levels were also assessed with enzyme-linked immunosorbent assay. The activation of astrocytes and microglia was evaluated through S100 staining and Western blot analysis of ionized calcium-binding adaptor molecule 1 respectively. Nuclear factor kappa-B (NF-κB) signaling was also evaluated by Western blot. Results: ICH mice demonstrated dramatic increase in mNSS, brain edema and cell apoptosis, indicating severe brain deficit. Fisetin treatment lowered these parameters, suggesting the alleviation of brain injury. Levels of proinflammatory cytokines were reduced, accompanied by a prominent decrease in activated astrocytes and microglia. NF-κB signaling was also attenuated by fisetin treatment. Conclusion: Fisetin effectively alleviates ICH by downregulating proinflammatory cytokines and attenuating NF-κB signaling. These data suggest fisetin as a valuable natural flavonol for clinical management of ICH-induced brain injury.

Effect of Different Aβ Aggregates as Antigen on the Measure of Naturally Occurring Autoantibodies against Amyloid-β40/42 in IVIG

2020 ◽  
Vol 16 (14) ◽  
pp. 1290-1299
Author(s):  
Haijun Cao ◽  
Xi Du ◽  
Renyong Zeng ◽  
Zhaoji Lv ◽  
Shengliang Ye ◽  
...  
Keyword(s):  
Statistical Analysis ◽  
Western Blot ◽  
Intravenous Immunoglobulin ◽  
Immunosorbent Assay ◽  
Amyloid Β ◽  
Enzyme Linked Immunosorbent Assay ◽  
Nonspecific Binding ◽  
Naturally Occurring ◽  
High Level ◽  
The Impact

Background: The specific Intravenous Immunoglobulin (IVIG) for Alzheimer’s Disease (AD) is developing, which contains a high level of naturally occurring autoantibodies against amyloid-β (nAbs-Aβ), and the measure of nAbs-Aβ content is greatly essential. Though Enzyme-Linked Immunosorbent Assay (ELISA) has been widely used in detecting the nAbs-Aβ content, the impact of Aβ aggregates species chosen as antigen in ELISA on this measure has not been evaluated. Objective: To clarify the influence of different Aβ40/42 aggregates as antigen during ELISA on the content of nAbs-Aβ40/42 measured in IVIG. Method: Preparation of various Aβ40/42 aggregates was performed by different aggregation solutions and various lengths of time, and analyzed by western blot. Different Aβ40/42 aggregates as antigen were adopted to measure the nAbs-Aβ40/42 content in IVIG by ELISA, and the control was carried out to reduce interference of nonspecific binding. The Bonferroni and Dunnett’s T3 were used for statistical analysis. Results: The duration for the formation of Aβ40/42 aggregates had more effect on detecting nAbs-Aβ40/42 content in IVIG than the aggregation solution. Higher content of nAbs-Aβ40/42 in the same IVIG was displayed when measured with Aβ40/42 aggregates at day 3, instead of at day 0.5 and day 7.0. The nAbs- Aβ40/42 contents in the same IVIG measured with Aβ40/42 aggregates prepared in different solutions were obviously different, but there was no significant regularity among them. Conclusion: The nAbs-Aβ40/42 content in the same IVIG is significantly different when measured with Aβ40/42 aggregated under different conditions. The nAbs-Aβ40/42 content in IVIG by antigen-dependent measures, like ELISA, is uncertain.

scholarly journals Murine Gammaherpesvirus 68 Pathogenesis Is Independent of Caspase-1 and Caspase-11 in Mice and Impairs Interleukin-1β Production upon Extrinsic Stimulation in Culture

2015 ◽  
Vol 89 (13) ◽  
pp. 6562-6574 ◽  
Author(s):  
Brandon Cieniewicz ◽  
Qiwen Dong ◽  
Gang Li ◽  
James C. Forrest ◽  
Bryan C. Mounce ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Interleukin 1Β ◽  
Interferon Response ◽  
Cell Infection ◽  
Murine Gammaherpesvirus ◽  
Caspase 1 ◽  
Gammaherpesvirus 68 ◽  
Murine Gammaherpesvirus 68 ◽  
The Impact

ABSTRACTGammaherpesviruses establish lifelong infections that are associated with the development of cancer. These viruses subvert many aspects of the innate and adaptive immune response of the host. The inflammasome, a macromolecular protein complex that controls inflammatory responses to intracellular danger signals generated by pathogens, is both activated and subverted during human gammaherpesvirus infection in culture. The impact of the inflammasome response on gammaherpesvirus replication and latencyin vivois not known. Caspase-1 is the inflammasome effector protease that cleaves the proinflammatory cytokines interleukin-1β (IL-1β) and IL-18. We infectedcaspase-1-deficient mice with murine gammaherpesvirus 68 (MHV68) and observed no impact on acute replication in the lung or latency and reactivation from latency in the spleen. This led us to examine the effect of viral infection on inflammasome responses in bone marrow-derived macrophages. We determined that infection of macrophages with MHV68 led to a robust interferon response but failed to activate caspase-1 or induce the secretion of IL-1β. In addition, MHV68 infection led to a reduction in IL-1β production after extrinsic lipopolysaccharide stimulation or upon coinfection withSalmonella entericaserovar Typhimurium. Interestingly, this impairment occurred at the proIL-1β transcript level and was independent of the RTA, the viral lyticreplication andtranscriptionactivator. Taken together, MHV68 impairs the inflammasome response by inhibiting IL-1β production during the initial stages of infection.IMPORTANCEGammaherpesviruses persist for the lifetime of the host. To accomplish this, they must evade recognition and clearance by the immune system. The inflammasome consists of proteins that detect foreign molecules in the cell and respond by secreting proinflammatory signaling proteins that recruit immune cells to clear the infection. Unexpectedly, we found that murine gammaherpesvirus pathogenesis was not enhanced in mice lackingcaspase-1, a critical inflammasome component. This led us to investigate whether the virus actively impairs the inflammasome response. We found that the inflammasome was not activated upon macrophage cell infection with murine gammaherpesvirus 68. Infection also prevented the host cell inflammasome response to other pathogen-associated molecular patterns, indicated by reduced production of the proinflammatory cytokine IL-1β upon bacterial coinfection. Taken together, murine gammaherpesvirus impairment of the inflammatory cytokine IL-1β in macrophages identifies one mechanism by which the virus may inhibit caspase-1-dependent immune responses in the infected animal.

Probiotics exert reciprocal effects on autophagy and interleukin-1β expression in Salmonella-infected intestinal epithelial cells via autophagy-related 16L1 protein

2019 ◽  
Vol 10 (8) ◽  
pp. 913-922 ◽  
Author(s):  
W.-T. Lai ◽  
F.-C. Huang
Keyword(s):  
Epithelial Cells ◽  
Protein Expression ◽  
Western Blot ◽  
Inflammatory Responses ◽  
Intestinal Epithelial Cells ◽  
Bifidobacterium Longum ◽  
Lactobacillus Rhamnosus ◽  
Interleukin 1Β ◽  
Intestinal Epithelial ◽  
Serovar Typhimurium

This study aimed to examine how probiotics affect autophagy and interleukin-1β (IL-1β) expression in Salmonella-infected intestinal epithelial cells (IECs). The original Caco-2 cells and ATG16L1 siRNA-transfected Caco-2 cells were pretreated or left untreated with probiotics, including Lactobacillus rhamnosus GG (LGG; ATCC 53103) and Bifidobacterium longum (BL; ATCC15697), and these cells were infected with wild-type Salmonella enterica serovar Typhimurium (S. Typhimurium strain, SL1344). Western blot analysis was used to detect the conversion of microtubule-associated proteins 1A/1B light chain 3B (LC3)-I to LC3-II. Immunofluorescence was used to analyse LC3+ autophagosomes. Membrane proteins were analysed by western blot for protein (ATG16L1, NOD2), and total RNA by RT-PCR for mRNA expression [ATG16L1, vitamin D receptor (VDR)]. We demonstrated that probiotics enhanced both VDR mRNA, and nucleotide-binding oligomerisation domain-containing protein 2 (NOD2) and autophagy-related protein 16-like 1 (ATG16L1) protein expression. The enhanced expression resulted in autophagic LC3-II protein expression and formation of LC3 punctae in Salmonella-infected Caco-2 cells. It was observed that ATG16L1 siRNA could attenuate this mechanism, and ATG16L1-mediated IL-1β expression was suppressed by probiotics. These results suggest that probiotics enhance autophagy and also suppress inflammatory IL-1β expression in Salmonella-infected IECs via membrane ATG16L1 protein expression. Probiotics may enhance autophagic clearance of Salmonella infection and modulate inflammatory responses to protect the hosts. Hence, we can assume that probiotics could treat infectious and autoimmune diseases through mechanisms involving ATG16L1.

scholarly journals P2Y6 Receptor-Mediated Spinal Microglial Activation in Neuropathic Pain

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Jiang Bian ◽  
Ying Zhang ◽  
Yan Liu ◽  
Qun Li ◽  
Hai-bin Tang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Western Blot ◽  
Mrna Expression ◽  
Inflammatory Responses ◽  
Enzyme Linked Immunosorbent Assay ◽  
Sprague Dawley ◽  
Sham Surgery ◽  
P2y6 Receptor

Objective. To explore the role of purine family member P2Y6 receptors in regulating neuropathic pain (NP) via neuroinflammation in the spinal cord. Methods. Chronic constriction injury of the sciatic nerve (CCI) of NP was classic in setting up models on Sprague-Dawley (SD) rats. Experiments were performed on rats with sham surgery, CCI, CCI + MRS2578 (a P2Y6 receptor antagonist), and UDP (a P2Y6 receptor agonist). The hyperalgesia intensity was mirrored by paw withdrawal threshold (PWT) and thermal withdrawal latency (TWL). Immunofluorescence staining and western blot were used to evaluate activated microglial marker Iba-1. Enzyme-linked immunosorbent assay (ELISA) was used to access levels of IL-6. Conventional reverse transcription polymerase chain reaction (RT-PCR) and western blot analysis were used to detect the expression of P2Y6 mRNA and activation of JAK/STAT signaling. Results. Among all groups, CCI caused decreased PWT and TWL compared to sham surgery, meaning a successful establishment of the NP model. These decreased values of PWT and TWL tests could be prevented by intraperitoneally injected MRS2578 and enhanced by UDP administration. Similarly, CCI induced increase of Iba-1 protein, P2Y6 mRNA expression, and circulating IL-6 secretion, as well as increased JAK2/STAT3 mRNA expression and phosphorylating modification in spinal cord tissues could also be diminished by MRS2578 treatment and exacerbated by UDP. Conclusions. These findings indicated the crucial role of the P2Y6 receptor in modulating the microglial and inflammatory responses in the process of NP in vivo. Results from this study would provide insights into targeting the P2Y6 receptor to treat NP in the near future.

scholarly journals HMGB1 Inhibition to Ameliorate Organ Failure and Increase Survival in Trauma

2021 ◽  
Author(s):  
Zhangsheng Yang ◽  
Milomir O Simovic ◽  
Peter R Edsall ◽  
Bin Liu ◽  
Tomas S Cancio ◽  
...  
Keyword(s):  
Inflammatory Mediators ◽  
Plasma Levels ◽  
Injury Severity ◽  
Inflammatory Responses ◽  
High Mobility ◽  
Organ Damage ◽  
Blast Injury ◽  
Military Hospital ◽  
Remote Organ ◽  
Combat Casualties

Several preclinical and clinical reports have demonstrated that levels of circulating high mobility group box 1 protein (HMGB1) are increased early after trauma and are associated with systemic inflammation and clinical outcomes. However, the mechanisms of the interaction between HMGB1 and inflammatory mediators that lead to the development of remote organ damage after trauma remain obscure. HMGB1 and inflammatory mediators were analyzed in plasma from 54 combat casualties, collected on admission to a military hospital in Iraq, and at 8 and 24 hours after admission. Forty-five (83%) of these patients had traumatic brain injury (TBI). Nine healthy volunteers were enrolled as controls. HMGB1 plasma levels were significantly increased in the first 8 hours after admission, and were found to be associated with systemic inflammatory responses, injury severity score, and presence of TBI. These data provided the rationale for designing experiments in rats subjected to blast injury and hemorrhage, to explore the effect of HMGB1 inhibition by CX-01. Animals were cannulated, then recovered for 5-7 days before blast injury in a shock tube and volume-controlled hemorrhage. Blast injury and hemorrhage induced an early increase in HMGB1 plasma levels that coincided with severity of tissue damage and mortality. CX-01 inhibited systemic HMGB1 release, decreased local and systemic inflammatory responses, significantly reduced tissue and organ damage, and tended to increase survival. These data suggest that CX-01 has potential as an adjuvant treatment for traumatic hemorrhage.

scholarly journals HMGB1 Inhibition to Ameliorate Organ Failure and Increase Survival in Trauma

Biomolecules ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 101
Author(s):  
Zhangsheng Yang ◽  
Milomir O. Simovic ◽  
Peter R. Edsall ◽  
Bin Liu ◽  
Tomas S. Cancio ◽  
...  
Keyword(s):  
Inflammatory Mediators ◽  
Plasma Levels ◽  
Injury Severity ◽  
Inflammatory Responses ◽  
High Mobility ◽  
Organ Damage ◽  
Blast Injury ◽  
Military Hospital ◽  
Remote Organ ◽  
Combat Casualties

Several preclinical and clinical reports have demonstrated that levels of circulating high mobility group box 1 protein (HMGB1) are increased early after trauma and are associated with systemic inflammation and clinical outcomes. However, the mechanisms of the interaction between HMGB1 and inflammatory mediators that lead to the development of remote organ damage after trauma remain obscure. HMGB1 and inflammatory mediators were analyzed in plasma from 54 combat casualties, collected on admission to a military hospital in Iraq, and at 8 and 24 h after admission. In total, 45 (83%) of these patients had traumatic brain injury (TBI). Nine healthy volunteers were enrolled as controls. HMGB1 plasma levels were significantly increased in the first 8 h after admission, and were found to be associated with systemic inflammatory responses, injury severity score, and presence of TBI. These data provided the rationale for designing experiments in rats subjected to blast injury and hemorrhage, to explore the effect of HMGB1 inhibition by CX-01 (2-O, 3-O desulfated heparin). Animals were cannulated, then recovered for 5–7 days before blast injury in a shock tube and volume-controlled hemorrhage. Blast injury and hemorrhage induced an early increase in HMGB1 plasma levels that coincided with severity of tissue damage and mortality. CX-01 inhibited systemic HMGB1 activity, decreased local and systemic inflammatory responses, significantly reduced tissue and organ damage, and tended to increase survival. These data suggest that CX-01 has potential as an adjuvant treatment for traumatic hemorrhage.

scholarly journals LP-cs Ameliorated CCl 4 -Induced Acute Liver Injury by Suppression of Cellular Stress

2021 ◽  
Author(s):  
Zeping Xu ◽  
Xiaofeng Li ◽  
Yuying Li ◽  
Ping Wang ◽  
Junnan Wu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Lactobacillus Plantarum ◽  
Inflammatory Responses ◽  
Acute Liver Injury ◽  
Regulatory Protein ◽  
High Mobility ◽  
Serum Levels ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tunel Staining ◽  
Related Factor

Abstract Background: Acute liver injury (ALI) involves excessive oxidative stress(OS) and inflammatory responses, leading to a high mortality rate due to lack of effective therapy. Carbon tetrachloride (CCl4) is widely used to induce ALI by induction of reactive oxygen species. Probiotics, including Lactobacillus plantarum ST-III, have been shown to produce antibacterial and antioxidant substances such as organic acids or bacteriocins that reduce liver damage. Nevertheless, the effect of Lactobacillus plantarum ST-III culture supernatant (L-P-cs) on CCl4-induced liver injury remains unclear.Methods: Mice were pretreated with L-P-cs or medium for 14days before one dose of 0.2% CCl4 at 10ml/kg body weight delivered by intraperitoneal injection. CCl4-induced liver injury was examined by measuring serum levels of liver transaminases and high mobility-group box 1 protein (HMGB1) and liver histological staining. Inflammation and apoptosis in liver were evaluated by real-time PCR, enzyme-linked immunosorbent assay (ELISA), and TUNEL staining. Apoptosis in NCTC 1469 cells was detected using CCK8 and western blotting (WB). In liver, OS and endoplasmic reticulum stress(ERS)-related proteins were measured using kits and WB.Results: L-P-cs significantly ameliorated CCl4-induced liver injury and reduced CCl4- induced inflammatory response and apoptosis, consistent with NCTC 1469 cells' results. L-P-cs also restored CCl4-induced increases in cell OS and ERS to normalize liver function. Specifically, L-P-cs pretreatment decreased CCl4-induced increases in nuclear factor (erythroid-2 related) factor 2, HO-1, superoxide dismutase, glucose regulatory protein, and activating transcription factor 6.Conclusion: L-P-cs synergistically improves liver lobule necrosis, hepatocyte inflammation, and apoptosis by reducing liver OS and ERS.

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