scholarly journals Pyrroloquinoline Quinone Inhibits Rotenone-Induced Microglia Inflammation by Enhancing Autophagy

Molecules ◽  
2020 ◽  
Vol 25 (19) ◽  
pp. 4359
Author(s):  
Qi Zhang ◽  
Jing Zhou ◽  
Mi Shen ◽  
Hui Xu ◽  
Shu Yu ◽  
...  
Keyword(s):  
Cell Viability ◽  
Mitochondrial Dysfunction ◽  
Neuroprotective Effect ◽  
Pyrroloquinoline Quinone ◽  
Transmission Electron ◽  
Bv2 Cells ◽  
Mitochondrial Functions ◽  
Tnf Α ◽  
Bv2 Microglia ◽  
Factor Α

Neuroinflammation is a feature common to neurodegenerative diseases, such as Parkinson’s disease (PD), which might be responsive to therapeutic intervention. Rotenone has been widely used to establish PD models by inducing mitochondrial dysfunction and inflammation. Our previous studies have reported that pyrroloquinoline quinone (PQQ), a naturally occurring redox cofactor, could prevent mitochondrial dysfunction in rotenone induced PD models by regulating mitochondrial functions. In the present study, we aimed to investigate the effect of PQQ on neuroinflammation and the mechanism involved. BV2 microglia cells were pre-treated with PQQ followed by rotenone incubation. The data showed that PQQ did not affect the cell viability of BV2 cells treated with rotenone, while the conditioned medium (CM) of BV2 cells pre-treated with PQQ significantly increased cell viability of SH-SY5Y cells. In rotenone-treated BV2 cells, PQQ dose-dependently decreased lactate dehydrogenase (LDH) release and suppressed the up-regulation of pro-inflammation factors, such as interleukin-1β (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α) in the cultured media, as well as nitric oxide (NO) release induced by rotenone. PQQ pretreatment also increased the ratio of LC3-II/LC3-I and expression of Atg5 in BV2 cells stimulated with rotenone. Additionally, the autophagosome observed by transmission electron microscopy (TEM) and co-localization of mitochondria with lysosomes indicated that mitophagy was induced by PQQ in rotenone-injured BV2 cells, and the PINK1/parkin mediated mitophagy pathway was regulated by PQQ. Further, autophagy inhibitor, 3-methyladenine (3-MA), partially abolished the neuroprotective effect of PQQ and attenuated the inhibition of inflammation with PQQ pretreatment. Taken together, our data extend our understanding of the neuroprotective effect of PQQ against rotenone-induced injury and provide evidence that autophagy enhancement might be a novel therapeutic strategy for PD treatment.

T-614 inhibits human aortic adventitial fibroblast proliferation and promotes interleukin-8 production in vitro

Vascular ◽  
2019 ◽  
Vol 28 (3) ◽  
pp. 314-320
Author(s):  
Weiping Ci ◽  
Tian Wang ◽  
Taotao Li ◽  
Jin Wan
Keyword(s):  
Cell Viability ◽  
Vascular Wall ◽  
Underlying Mechanism ◽  
Interleukin 8 ◽  
Control Group ◽  
Survival Fraction ◽  
Tnf Α ◽  
Significant Difference ◽  
Factor Α

Objectives The effect and underlying mechanism of T-614 (iguratimod) on Takayasu’s arteritis (TA) are unknown. Here, we report the effects of T-614 on cell proliferation and interleukin-8 (IL-8) production in human aortic adventitial fibroblasts (HAAFs) in vitro and explore its initial benefit in terms of vascular wall inflammation and remodeling for patients with TA. Methods HAAFs were cultured with 0, 5, 50, 100, or 250 μg/ml T-614 in the absence or presence of tumor necrosis factor-α (TNF-α) in vitro. Cell viability was determined by a modified MTT assay. Supernatant IL-8 levels were measured by enzyme-linked immunosorbent assays. Results In the presence of TNF-α, compared to that in the control group, cell viability of HAAFs significantly decreased in the 50, 100, and 250 μg/ml T-614 treatment groups (OD value: P <  0.01, P <  0.001, P <  0.001, respectively; survival fraction (SF): P <  0.05, P <  0.001, P <  0.001, respectively). However, there was no significant difference in cell viability between TNF-α-stimulated and unstimulated groups at the same concentration of T-614. In the absence or presence of TNF-α, T-614 suppressed HAAF cell viability dose-dependently (OD value: r = −0.915, P =  0.000; r = −0.926, P =  0.000, respectively; SF: r = −0.897, P =  0.000; r = −0.885, P =  0.000, respectively). Compared to that in the control group, in the absence of TNF-α, IL-8 levels in the 5 and 100 μg/ml T-614-treated groups were significantly higher ( P <  0.05); in the presence of TNF-α, IL-8 levels in the 5, 50, and 100 μg/ml T-614-treated groups were significantly higher ( P <  0.001, P <  0.001, P <  0.01, respectively). Further, there was a negative correlation between supernatant IL-8 levels and T-614 concentration in groups stimulated with TNF-α ( r = −0.670, P =  0.000), but there was no significant correlation between these parameters in groups that were not stimulated with TNF-α. Conclusions In the absence or presence of TNF-α, T-614 can inhibit HAAF proliferation and promote IL-8 production in vitro; therefore, it could be used to prevent adventitial thickening of the aorta and improve vascular remodeling in inflammatory environments in vitro and might provide a new immunotherapeutic intervention for TA.

scholarly journals Ginsenoside Rc Protects Neurons From Oxygen-glucose Deprivation Injuries and Its Mechanistic Investigation via a Network Pharmacology-based Analysis

2020 ◽  
Author(s):  
Mingmin Huang ◽  
Shaoru Chen ◽  
Kening Zheng ◽  
Qu Liu ◽  
Kening Li ◽  
...  
Keyword(s):  
Molecular Docking ◽  
Cell Viability ◽  
Neuroprotective Effect ◽  
Glucose Deprivation ◽  
Network Pharmacology ◽  
Oxygen Glucose Deprivation ◽  
Cell Toxicity ◽  
Tnf Α ◽  
Neuron Damage ◽  
Ginsenoside Rc

Abstract Background: Ginsenoside Rc (Rc) is one of the major active components of Panax ginseng Meyer. Studies have shown that Rc has remarkable effect in protection of nervous system. However, the potential molecular mechanism of its neuroprotective effect remains unclear. Our study aim to investigate the neuroprotective effect of Rc on neuron damage and explore the potential mechanism on its regulation of TNF-α and DRP-1.Methods: Oxygen-glucose deprivation reperfusion (OGD/R) cell neuron damage modle was induced by Na2S2O4 and EBSS solution. After preventive administration, cell viability and cell toxicity were detected to evaluate the putative neuroprotective properties of Rc. Network pharmacology and molecular docking simulation studies were performed to predict the potential targets and pharmacological mechanism. Furthermore, the prediction was validated via western blot assay and specific antagonist. Results: In OGD/R injured cells, Rc significantly improved cell viability (Rc middle dose vs. OGD/R model: 67.3±2.33% vs. 55.7±1.14%, P<0.05) and obviously decreased cell toxicity (Rc middle dose vs. OGD/R model: 147±39.7% vs. 232±29.4%, P<0.01). Analysis of network pharmacology and molecular docking indicated that the key targets of Rc are TNF-α and DRP-1. Subsequently molecular biological studies showed a significant increase on expression of TNF-α and DRP-1 in model group. Conversely, administration of Rc reversed the alteration significantly and presented a dose dependence. By adding antagonist, we validated that Rc had an indirect regulation on TNF-α and DRP-1. Conclusions: Rc possess protective properties against OGD-induced neuron damage by regulating the expression of TNF-α and DRP-1.

scholarly journals Ergosterol of Cordyceps militaris Attenuates LPS Induced Inflammation in BV2 Microglia Cells

2015 ◽  
Vol 10 (6) ◽  
pp. 1934578X1501000 ◽  
Author(s):  
Neeranjini Nallathamby ◽  
Lee Guan-Serm ◽  
Sharmili Vidyadaran ◽  
Sri Nurestri Abd Malek ◽  
Jegadeesh Raman ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Viability ◽  
Ethyl Acetate ◽  
Ethyl Acetate Fraction ◽  
Cordyceps Militaris ◽  
No Production ◽  
Nitric Oxide Production ◽  
Cytotoxic Effects ◽  
Bv2 Cells ◽  
Bv2 Microglia

Different solvent extracts of Cordyceps militaris stroma powder were tested for cell viability and inhibition of nitric oxide (NO) production in lipopolysaccharide (LPS) triggered BV2 microglia cells. Chemical investigation of the ethyl acetate fraction resulted in an enriched ergosterol sub-fraction CE3. The BV2 cells showed no cytotoxic effects when treated with the ethyl acetate fraction and sub-fraction CE3 at concentrations of 0.1 μg/mL – 100 μg/mL compared with the control. At 10 μg/mL, the ethyl acetate fraction and sub-fraction CE3 had the highest reduction of 48.0% and 44.7% of nitric oxide production, respectively. The major compound in sub-fraction CE3 was ergosterol, identified by GCMS, and the purity was checked by HPLC. Further, the reduction of nitric oxide in LPS triggered BV2 cells was about three fold higher when compared with the control commercial ergosterol.

scholarly journals Isoorientin Inhibits Amyloid β25–35-Induced Neuronal Inflammation in BV2 Cells by Blocking the NF-κB Signaling Pathway

Molecules ◽  
2021 ◽  
Vol 26 (22) ◽  
pp. 7056
Author(s):  
Buyun Kim ◽  
Ki Yong Lee ◽  
Byoungduck Park
Keyword(s):  
Neurodegenerative Disorder ◽  
Drug Candidate ◽  
Therapeutic Drug ◽  
Treatment And Prevention ◽  
Bv2 Cells ◽  
Tnf Α ◽  
Underlying Mechanisms ◽  
Induced Apoptosis ◽  
Factor Α ◽  
The Brain

Alzheimer’s disease (AD) is a severe neurodegenerative disorder. AD is pathologically characterized by the formation of intracellular neurofibrillary tangles, and extracellular amyloid plaques which were comprised of amyloid-beta (Aβ) peptides. Aβ induces neurodegeneration by activating microglia, which triggers neurotoxicity by releasing various inflammatory mediators and reactive oxygen species (ROS). Nuclear factor-kappa B (NF-κB) is expressed in human tissues including the brain and plays an important role in Aβ-mediated neuronal inflammation. Thus, the identification of molecules that inhibit the NF-κB pathway is considered an attractive strategy for the treatment and prevention of AD. Isoorientin (3′,4′,5,7-Tetrahydroxy-6-C-glucopyranosyl flavone; ISO), which can be extracted from several plant species, such as Philostachys and Patrinia is known to have various pharmacological activities such as anticancer, antioxidant, and antibacterial activity. However, the effect of ISO on Aβ-mediated inflammation and apoptosis in the brain has yet to be elucidated. In the present study, we investigated whether ISO regulated Aβ-induced neuroinflammation in microglial cells and further explored the underlying mechanisms. Our results showed that ISO inhibited the expression of iNOS and COX-2 induced by Aβ25–35. And, it inhibited the secretion of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). In addition, ISO reduced the ROS production in Aβ25–35-induced BV2 cells and inhibited NF-κB activation. Furthermore, ISO blocked Aβ25–35-induced apoptosis of BV2 cells. Based on these findings, we suggest that ISO represents a promising therapeutic drug candidate for the treatment and prevention of AD.

scholarly journals Alprostadil attenuates LPS-induced cardiomyocyte injury by inhibiting the Wnt5a/JNK/NF-κB pathway

Herz ◽  
2019 ◽  
Vol 45 (S1) ◽  
pp. 130-138 ◽  
Author(s):  
T. Yu ◽  
D. Dong ◽  
J. Guan ◽  
J. Sun ◽  
M. Guo ◽  
...  
Keyword(s):  
Cell Viability ◽  
Mrna Expression ◽  
Molecular Mechanisms ◽  
Quantitative Polymerase Chain Reaction ◽  
Cellular Damage ◽  
H9c2 Cells ◽  
Tnf Α ◽  
H9c2 Cardiomyocytes ◽  
Anti Inflammatory ◽  
Factor Α

Abstract Background Clinical research has demonstrated that alprostadil has an anti-inflammatory effect; however, to date, its molecular mechanisms remain unclear. This study aimed to examine the anti-inflammatory activity and related mechanisms of alprostadil in lipopolysaccharide (LPS)-treated H9c2 cells. Methods Cell morphology was observed under an inverted light microscope, while cell viability was assessed with the 3‑(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) assay. Enzyme-linked immunosorbent assays (ELISA) were conducted to study biochemical indicators of cellular damage, such as released lactate dehydrase (LDH) and troponin, and inflammatory cytokine levels including interleukin-1β (IL-1β), IL-6, IL-17, and tumor necrosis factor-α (TNF-α). The mRNA expression levels of Wnt5a, c‑jun N‑terminal kinase (JNK), and nuclear factor kappa B (NF-κB) were further investigated by real-time quantitative polymerase chain reaction (RT-PCR). The effects of alprostadil on the Wnt5a/JNK/NF-κB pathway in H9c2 cells was examined by Western blotting. Results Alprostadil increased the cell viability of LPS-stimulated H9c2 cells, reduced LDH and troponin production, and attenuated IL-1β, IL-6, IL-17, and TNF-α secretion. Moreover, alprostadil reduced the mRNA expression of Wnt5a, JNK, and NF-κB and decreased the expression of Wnt5a, NF-κB, and the ratio of p‑JNK/JNK in H9c2 cells treated with LPS. The siWnt5a or JNK inhibitor SP600125 significantly augmented the inhibitory effects of alprostadil on the Wnt5a/JNK/NF-κB pathway. Conclusion Our results show that alprostadil has anti-inflammatory effects and could attenuate LPS-induced injury in H9c2 cardiomyocytes via the Wnt5a/JNK/NF-κB pathway.

scholarly journals Gualou Guizhi Granule Suppresses LPS-induced Inflammatory Response of Microglia and Protects Against Microglial-Mediated Neurotoxicity in HT22 via Akt/NF-κB Signaling Pathways

2020 ◽  
Author(s):  
Yuqin Zhang ◽  
Yaojun Liu ◽  
Liming Fan ◽  
Lihong Nan ◽  
Wei Xu ◽  
...  
Keyword(s):  
Conditioned Medium ◽  
Neuronal Apoptosis ◽  
Neuroprotective Effect ◽  
Microglial Cells ◽  
Nuclear Factor ◽  
Ht22 Cells ◽  
Nuclear Factor Kappa ◽  
Bv2 Cells ◽  
Bv2 Microglia ◽  
Bv2 Microglial Cells

Abstract Background Neuroinflammation plays a crucial part in the commence and advancement of ischemic stroke. Gualou Guizhi Granule (GLGZG) is known to exhibit well neuroprotective effect, but it is not known whether GLGZG can regulate inflammatory process at the cellular level in BV2 microglia cells and protect against microglial-mediated neurotoxicity in neurons. Herein, we aimed to investigate the anti-inflammatory effects of GLGZG on BV2 microglia cells and protection against microglial-mediated neurotoxicity in neurons. Methods Cell model of neuroinflammation was constructed by lipopolysaccharide (LPS) to observe the effect of GLGZG in the presence or absence of GLGZG. The production of nitric oxide (NO), inflammatory mediators were detected. Moreover, potential mechanisms associated with anti-inflammatory effect, such as inhibition of microglial activation, the nuclear factor kappa B (NF-κB) were also investigated. In addition, to prove whether GLGZG protects against microglial-mediated neurotoxicity, neuronal HT22 cells were cultured in conditioned medium. And cell survivability, neuronal apoptosis of HT22 were evaluated. Results It was found that a main regulator of inflammation, NO, is suppressed by GLGZG in BV2 microglial cells. Moreover, GLGZG dose-dependently decreased the mRNA and protein levels of inducible NO synthase (iNOS) in LPS-stimulated BV2 cells. Additionally, GLGZG inhibited the expression and secretion of proinflammatory cytokines in BV2 microglial cells. And, GLGZG inhibited LPS-activated nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in BV2 microglial cells at the intracellular level. GLGZG negatively affected Akt phosphorylation: phosphorylated forms of Akt decreased. To check whether GLGZG protects against microglial-mediated neurotoxicity, neuronal HT22 cells were incubated in the conditioned medium. GLGZG showed a neuroprotective effect by promoting cell survivability, suppressing neuronal apoptosis. Conclusions GLGZG exerted its potential effects on suppressing inflammatory responses in LPS-induced BV2 cells by attenuating NF-κB and Akt pathways. In addition, GLGZG could protect against microglial-mediated neurotoxicity in HT22.

scholarly journals The impact of pretreatment with simvastatin on kidney tissue of rats with acute sepsis

2017 ◽  
Vol 104 (2) ◽  
pp. 158-170 ◽  
Author(s):  
E Özkök ◽  
H Yorulmaz ◽  
G Ateş ◽  
I Aydın ◽  
M Ergüven ◽  
...  
Keyword(s):  
Enzyme Activities ◽  
Kidney Tissue ◽  
Thiobarbituric Acid ◽  
Histological Structure ◽  
Tubular Damage ◽  
Mitochondrial Enzyme ◽  
Mitochondrial Functions ◽  
Tnf Α ◽  
Factor Α ◽  
The Impact

It has been reported that changes in cytokine levels affect mitochondrial functions, levels of hypoxia-inducible factor α (HIF-1α), and tissue damage during sepsis. We aimed to investigate the effects of simvastatin pretreatment on mitochondrial enzyme activities, and on levels of ghrelin, HIF-1α, and thiobarbituric acid reactive substances (TBARS) in kidney tissue during sepsis. Rats were separated into four groups, namely, control, lipopolysaccharides (LPS) (20 mg/kg), simvastatin (20 mg/kg), and simvastatin + LPS. We measured the levels of mitochondrial enzyme activities and TBARS in the kidney using spectrophotometry. The histological structure of the kidney sections was examined after staining with hematoxylin and eosin. Tumor necrosis factor α (TNF-α), IL-10, HIF-1α, and ghrelin immunoreactivity were examined using proper antibodies. In tissue, TNF-α (p < 0.01) and HIF-1α (p < 0.05) levels were increased in the simvastatin + LPS and LPS groups. TBARS levels were higher in the LPS group than in the other groups (p < 0.01), but they were similar in the simvastatin + LPS and control groups (p > 0.05). Ghrelin immunoreactivity was lower in the LPS group (p < 0.05) and higher in the simvastatin + LPS group than in the LPS group (p < 0.01). We observed tubular damage in the sections of the LPS group. There were no differences in mitochondrial enzyme activities between the groups (p > 0.05). We observed that pretreatment of simvastatin caused favorable changes on ghrelin and TBARS levels in rats with sepsis.

Ulinastatin alleviates mitochondrial damage and cell apoptosis induced by isoflurane in human neuroglioma H4 cells

2020 ◽  
Vol 39 (10) ◽  
pp. 1417-1425
Author(s):  
D Lin ◽  
X Zhu ◽  
J Li ◽  
Y Yao ◽  
M Guo ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Structural Changes ◽  
Mitochondrial Damage ◽  
Structure Damage ◽  
Transmission Electron ◽  
Transport Chain ◽  
Tnf Α ◽  
Amyloid Aβ ◽  
Factor Α ◽  
Necrosis Factor

Isoflurane has been demonstrated to induce mitochondrial damage and cell apoptosis. The isoflurane-induced inflammation may be an important reason for this phenomenon. Studies have shown that ulinastatin (UTI) has an anti-inflammatory effect. Our aim was to investigate whether UTI could attenuate isoflurane-induced mitochondrial damage and cell apoptosis by inhibiting inflammation. Human neuroglioma H4 cells were exposed to isoflurane with or without UTI. The ratio of cell apoptosis was evaluated by flow cytometry. β-Amyloid (Aβ) peptide and cleaved caspase 3 expression were evaluated by Western blot analysis. The concentrations of tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) were detected by sandwich enzyme-linked immunosorbent assays. Mitochondrial structural changes were detected by transmission electron microscopy. Mitochondrial membrane potential (Δψm) was determined by 5,5′,6,6′-Tetrachloro-1,1′,3,3′-tetraethyl-imidacarbocyanine iodide (JC-1). The activity of the mitochondrial electron transport chain (ETC) complexes I, II, III, and IV was determined by assay kits. UTI attenuated the TNF-α and IL-1β release induced by isoflurane. UTI could also reduce mitochondrial structure damage, mitigate the decrease in Δψm, and improve ETC complexes dysfunction. Furthermore, it decreased cell apoptosis induced by isoflurane in H4 cells. UTI had no effect on isoflurane-induced Aβ expression. UTI may mitigate isoflurane-induced mitochondrial damage and cytotoxicity by inhibiting inflammation.

scholarly journals The Possible Neuroprotective Effect of Silymarin against Aluminum Chloride-Prompted Alzheimer’s-Like Disease in Rats

2020 ◽  
Vol 10 (9) ◽  
pp. 628 ◽  
Author(s):  
Hanaa R. Aboelwafa ◽  
Attalla F. El-kott ◽  
Eman M. Abd-Ella ◽  
Hany N. Yousef
Keyword(s):  
Aluminum Chloride ◽  
Pyramidal Neurons ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Nerve Fibers ◽  
Ultrastructural Changes ◽  
Neuroprotective Effects ◽  
Myelinated Nerve ◽  
Tnf Α ◽  
Factor Α

Alzheimer’s disease (AD) is a worldwide rapidly growing neurodegenerative disease. Here, we elucidated the neuroprotective effects of silymarin (SM) on the hippocampal tissues of aluminum chloride (AlCl3)-induced Alzheimer-like disease in rats using biochemical, histological, and ultrastructural approaches. Forty rats were divided into control, SM, AlCl3, and AlCl3 + SM groups. Biochemically, AlCl3 administration resulted in marked elevation in levels of lipid peroxidation (LPO) and nitric oxide (NO) and decrease in levels of reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD). Moreover, AlCl3 significantly increased tumor necrosis factor-α (TNF-α), interleukin-1beta (IL-1β), and acetylcholinesterase (AChE) activities. Furthermore, myriad histological and ultrastructural alterations were recorded in the hippocampal tissues of AlCl3-treated rats represented as marked degenerative changes of pyramidal neurons, astrocytes, and oligodendrocytes. Additionally, some myelinated nerve fibers exhibited irregular arrangement of their myelin coats, while the others revealed focal degranulation of their myelin sheaths. Severe defects in the blood–brain barrier (BBB) were also recorded. However, co-administration of SM with AlCl3 reversed most of the biochemical, histological, and ultrastructural changes triggered by AlCl3 in rats. The results of the current study indicate that SM can potentially mend most of the previously evoked neuronal damage in the hippocampal tissues of AlCl3-kindled rats.

scholarly journals Xuebijing inhibit inflammation, oxidative stress and promote apoptosis in human synovial cells via inhibition of MEK1/2 and NF-ĸB pathway

2021 ◽  
pp. 1-9
Author(s):  
Liang Li ◽  
Yafeng Li ◽  
Da Shi ◽  
Huajian Liu ◽  
Baohui Wang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Cell Viability ◽  
Cell Line ◽  
Treated Group ◽  
Synovial Cells ◽  
Joint Deformity ◽  
Tnf Α ◽  
Factor Α ◽  
And Oxidative Stress

Abstract Rheumatoid arthritis (RA) is categorized as an autoimmune disease that leads to bone or joint deformity due to altered immune response. Studies have concluded the role of inflammation and oxidative stress in the progression of RA and agents inhibiting these processes showed benificial effect against the disease. Xuebijing (XBJ) injection is an intravenous patent preparation made from five-traditional Chinese medicines. Previous studies showed its excellent pharmacological activities, such as against sepsis, inflammation, and oxidative stress which has encouraged us to investigate the protective effect of XBJ against rheumatoid arthritis cell line (MH7A). For this purpose, the effect of XBJ was quantified on several parameters on the human synovial MH7A cell line activated with tumor necrosis factor-α (TNF-α). The results of the study showed that the level of tested interleukines (IL- 1β, IL- 6, IL- 8) and collagenases 1, and 13, and matrix metallo-proteinases 1, and 13 (MMP-1, and MMP-13) were found significantly reduced in XBJ treated group as compared to TNF-α treated MH7A cells. The XBJ treated group showed reduction in mRNA protein expression of COX-2 and iNOS in RT-qPCR assay. The rate of cellular apoptosis was found increased in XBJ treated group with reduction of cell viability of MH7A cells. The XBJ also showed attenuation of the expression of p-MEK/1/2 and p-p65 in MH7A cells in a western blot analysis. Our results demonstrated that XBJ significantly inhibits the inflammatory response, prevents cell viability, and induces apoptosis in human RA synovial cells by preventing the activation of the MEK/NF-κB pathway.

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