scholarly journals Serum Inflammatory Factors and Oxidative Stress Factors Are Associated With Increased Risk of Frailty and Cognitive Frailty in Patients With Cerebral Small Vessel Disease

2022 ◽  
Vol 12 ◽  
Author(s):  
Lei Mu ◽  
Limin Jiang ◽  
Juan Chen ◽  
Mei Xiao ◽  
Wei Wang ◽  
...  

Objective: To study the correlation between serum inflammatory factors, oxidative stress factors and frailty, and cognitive frailty in patients with cerebral small vessel disease (CSVD).Methods: A total of 281 patients with CSVD were selected from Tianjin Huanhu Hospital and Inner Mongolia People's Hospital from March 2019 to March 2021. CSVD was diagnosed by MRI. The FRAIL scale was used to evaluate the frailty of patients. Patients with CSVD with frailty and MMSE score <27 were considered to have cognitive frailty. Patients with non-cognitive frailty were included in the control group. The Montreal Cognitive Assessment (MoCA) and Mini-Mental State Examination (MMSE) were used to evaluate the cognitive function of patients with CSVD. The serum interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-α), matrix metalloproteinase 3 (MMP-3), superoxide dismutase (SOD), and malondialdehyde (MDA) of patients with CSVD were detected. The correlation between blood inflammatory factors and oxidative stress factors with the frailty and cognitive frailty patients of CSVD were analyzed. Univariate and multivariate logistic regression were used to analyze the correlation between cognitive frailty and CSVD.Results: Among the patients with CSVD selected in this study, female patients and older patients had a higher proportion of frailty (p < 0.001). In the Frail group, MoCA score and MMSE score were significantly lower than in the Pre-Frail and Robust groups, Hamilton Depression Scale (HAMD) and Hamilton Anxiety Scale (HAMA) scores were significantly higher than the Pre-Frail and Robust groups, and the differences were statistically significant (p < 0.05). Serum CRP, IL-6, TNF-α, MMP-3, and MDA levels in the Frail group were higher, but SOD levels were lower. The levels of serum CRP, IL-6, TNF-α, MMP-3, and MDA in patients with CSVD in the Cognitive Frailty group were significantly higher than those of the Control group, while the levels of SOD were significantly lower than those of the Control group, and the differences were significant (p < 0.001). The results of univariate and multivariate logistic regression analysis showed that CRP, TNF-α, MMP-3, and MDA levels were associated with cognitive frailty in patients with CSVD (p < 0.05).Conclusion: The increase of serum CRP, TNF-α, MMP-3, and MDA levels are significantly related to the increased risk of frailty and cognitive frailty in patients with CSVD.

Author(s):  
Bijan Helli ◽  
Hadis Gerami ◽  
Maria Kavianpour ◽  
Habib Heybar ◽  
Seyed Kianoosh Hosseini ◽  
...  

Background: Curcumin demonstrated many pharmacological effects including antioxidants, anti-inflammation, eliminating free radicals, anti-tumor, lipid regulation, and anti-coagulation. Objective: This study aimed to assess and compare curcumin and nano-curcumin effects on lipid profile, oxidative stress, and inflammatory factors related to patients ‘heart. Method: This randomized, double-blind, placebo-controlled clinical trial was conducted on 90 patients undergoing coronary elective angioplasty which were randomly divided into 3 groups. The doses administered for 8 weeks were a 500 mg capsule of curcumin daily for the first group and an 80 mg capsule of nano-curcumin for the second group. However, the placebo group received capsules like curcumin. Lipid profile, oxidative stress factors, and inflammatory markers were measured at the baseline and end of the experiment. Results: Statistically significant changes were observed in the total cholesterol (TC), triacylglycerol (TG) and low-density lipoprotein cholesterol (LDL-C) in the intervention groups to the control group (p<0.05). Curcumin and nano-curcumin supplementation also improved significant changes in plasma levels of total antioxidant capacity (TAC), malondialdehyde (MDA), Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), high-sensitivity C-reactive protein (hs-CRP), Interleukin 1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) in comparison to the placebo (p<0.05). Furthermore, the nano-curcumin group compared to the curcumin group demonstrated significant changes (p<0.05) in TC, TG, SOD, MDA and TNF-α levels. Conclusion: The effects of curcumin on nano formula may be better for cardiac patients due to its high bioavailability.


Author(s):  
Min Dai ◽  
◽  
Cheng Peng ◽  

Methicillin-Resistant Staphylococcus Aureus (MRSA) is one of the most serious health concerns bacterial owing to its incidence and the severity of the associated infections. It is necessary to find new chemical compounds with anti-MRSA activity. A model of MRSA infection was prepared by intraperitoneal injection of MRSA. A. tasao-ko essential oil was used for pretreatment and treatment of MRSA-infected animals and the 50% effective dose (ED50) was calculated according to improved Karber’s method respectively. The levels of serum interleukin (IL)-1β, IL-6, Tumor Necrosis Factor alpha (TNF-α), Malondialdehyde (MDA), Glutathione Peroxidase (GSH-Px) and Hydroxyl Radical (·OH) were measured using dedicated assay kits. The statistical analysis of inflammatory factors and oxidative stress factors was tested using one-way ANOVA computed by SPSS software. The ED50 values for the prevention and treatment of MRSA infection in A. tasao-ko essential oil were 0.15 g/kg and 0.18 g/kg, respectively. A. tasao-ko essential oil significantly reduced the inflammatory factors (IL-1β, IL-6, TNF-α), oxidative stress factors (MDA, ·OH) and increased the GSH-Px content in mice infected with MRSA. In the high-dose group, 7 days after treatment, the cytokine contents have no difference with control group (P > 0.05). A. tasao-ko essential oil exhibited anti-MRSA effect in vivo and can also ameliorate the abnormal changes in inflammatory factors and oxidative stress that arise from MRSA.


Author(s):  
Hong Wang ◽  
Wenjuan Zhang ◽  
Jinren Liu ◽  
Junhong Gao ◽  
Le Fang ◽  
...  

Abstract Blast lung injury (BLI) is the major cause of death in explosion-derived shock waves; however, the mechanisms of BLI are not well understood. To identify the time-dependent manner of BLI, a model of lung injury of rats induced by shock waves was established by a fuel air explosive. The model was evaluated by hematoxylin and eosin staining and pathological score. The inflammation and oxidative stress of lung injury were also investigated. The pathological scores of rats’ lung injury at 2 h, 24 h, 3 days, and 7 days post-blast were 9.75±2.96, 13.00±1.85, 8.50±1.51, and 4.00±1.41, respectively, which were significantly increased compared with those in the control group (1.13±0.64; P&lt;0.05). The respiratory frequency and pause were increased significantly, while minute expiratory volume, inspiratory time, and inspiratory peak flow rate were decreased in a time-dependent manner at 2 and 24 h post-blast compared with those in the control group. In addition, the expressions of inflammatory factors such as interleukin (IL)-6, IL-8, FosB, and NF-κB were increased significantly at 2 h and peaked at 24 h, which gradually decreased after 3 days and returned to normal in 2 weeks. The levels of total antioxidant capacity, total superoxide dismutase, and glutathione peroxidase were significantly decreased 24 h after the shock wave blast. Conversely, the malondialdehyde level reached the peak at 24 h. These results indicated that inflammatory and oxidative stress induced by shock waves changed significantly in a time-dependent manner, which may be the important factors and novel therapeutic targets for the treatment of BLI.


2019 ◽  
Vol 35 (1) ◽  
Author(s):  
Ju-Bin Kang ◽  
Dong-Ju Park ◽  
Murad-Ali Shah ◽  
Myeong-Ok Kim ◽  
Phil-Ok Koh

Abstract Lipopolysaccharide (LPS) acts as an endotoxin, releases inflammatory cytokines, and promotes an inflammatory response in various tissues. This study investigated whether LPS modulates neuroglia activation and nuclear factor kappa B (NF-κB)-mediated inflammatory factors in the cerebral cortex. Adult male mice were divided into control animals and LPS-treated animals. The mice received LPS (250 μg/kg) or vehicle via an intraperitoneal injection for 5 days. We confirmed a reduction of body weight in LPS-treated animals and observed severe histopathological changes in the cerebral cortex. Moreover, we elucidated increases of reactive oxygen species and oxidative stress levels in LPS-treated animals. LPS administration led to increases of ionized calcium-binding adaptor molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) expression. Iba-1 and GFAP are well accepted as markers of activated microglia and astrocytes, respectively. Moreover, LPS exposure induced increases of NF-κB and pro-inflammatory factors, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Increases of these inflammatory mediators by LPS exposure indicate that LPS leads to inflammatory responses and tissue damage. These results demonstrated that LPS activates neuroglial cells and increases NF-κB-mediated inflammatory factors in the cerebral cortex. Thus, these findings suggest that LPS induces neurotoxicity by increasing oxidative stress and activating neuroglia and inflammatory factors in the cerebral cortex.


2017 ◽  
Vol 30 (3) ◽  
pp. 19
Author(s):  
Layla Abd-Al-Sattar Sadiq Laylani

  This study was designed to show, the role of Carthamus tinctorius safflower aqueous extract against toxicity of nickel chloride (NiCl2). Twenty male, rabbits were used and divided into four groups (with 5 rabbits in each group); group (control group) received normal diet, group II received orally 100mg/kg NiCl2 for six weeks, group III received 100mg/kg NiCl2 and 100mg/kg extract six weeks, group IV received 100mg/kg NiCl2 and 200mg/ kg extract six weeks. Hematological parameters showed (RBC (Red blood cells), Hb (Hemoglobin), PCV (Packed cells volume) decreased and WBC (White blood cells) increased) significant changes (P < 0.05) compared with control group. Immunological parameters (IgG, IgA and IgM increased) and oxidative stress factors (MDA increased and GSH decreased) show significant changes (P < 0.05) compared with control group. While, safflower aqueous adverse the negative effects of NiCl2 and causing ameliorative effects on all hematological parameters, hematological immunological parameters and oxidative stress factors showed no significant changes (P < 0.05) compared with control group. It was concluded that flower extract of Carthamus tinctorius has been antioxidant role against nickel chloride toxicity in rabbits.  


2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Rana M. Alhusayan ◽  
Badr Abdullah Aldahmash ◽  
Doaa M. El-Nagar ◽  
Ahmad Rady ◽  
Khalid Elfakki Ibrahim ◽  
...  

The liver is the most vital organ that could be influenced by inducers of hypersensitivity such as ovalbumin. The current study was carried out to explore the effects of butterbur (Petasites hybridus) extract on the ovalbumin-induced liver hypersensitivity in Swiss albino male mice. Animals were divided into 4 groups, 1st group served as a control group, 2nd group treated with daily oral administration of 75 mg/kg of butterbur extract, 3rd group received single oral dose 100 mg/kg of ovalbumin to induce hypersensitivity, and 4th group treated with oral administration of butterbur extract one-day post to the hypersensitivity induction. Ovalbumin induces a significant increase in the activity of liver enzymes and MDA and decreased the activity of CAT after the ovalbumin treatment. Histopathological investigations revealed marked pathological alterations in liver tissues in the form of hyaline degeneration and fibrosis. Additionally, heavy immune response indicated by immunostaining of MDA and TNF-α could be observed. In contrast, posttreatment with butterbur extract after hypersensitivity induction resulted in a significant decrease of liver enzymes and oxidative stress and reduced the inflammation and fibrosis of liver tissues. These results suggest that butterbur extract is considered as anti-inflammatory and antioxidant therapeutic herb for hypersensitivity treatment of liver.


2019 ◽  
Vol 8 (2) ◽  
pp. 146-152 ◽  
Author(s):  
Ali Nouri ◽  
Esfandiar Heidarian

Introduction: Diclofenac (DIC), a phenylacetic acid compound which belongs to nonsteroidal anti-inflammatory drugs (NSAIDs), is generally used for the treatment of various diseases such as rheumatoid arthritis, ankylosing spondylitis, acute muscle pain conditions and osteoarthritis. Overdose of DIC can lead to renal injuries in both experimental animal and human. Our research was done to assess the protective role of silymarin on renal damage induced by DIC in rats. Methods: Thirty-two Wistar rats were assigned to four groups (n=8/group). Group 1 was control group; animals in group 2 were administrated DIC; Groups 3 and 4 administrated DIC plus silymarin with doses of 100 mg/kg and 200 mg/kg, orally (p.o), respectively. Various biochemical, molecular, and histological parameters were evaluated in serum and tissue homogenate. Results: In the second group, the levels of kidney catalase (CAT), vitamin C and superoxide dismutase (SOD) remarkably reduced (P < 0.05) relative to the control group. Also, urea, creatinine (Cr), malondialdehyde (MDA), serum tumor necrosis factor-α (TNF-α) and gene expression of TNF-α in this group were noticeably elevated (P < 0.05) relative to the control group. Treatment with silymarin caused a remarkable elevation (P < 0.05) in vitamin C, SOD, CAT and a remarkable reduction (P < 0.05) in the content of MDA, urea, Cr, TNF-α gene expression and serum TNF-α in comparison with second group. Histological injuries were also ameliorated by silymarin administration. Conclusion: The results confirm that silymarin has an ameliorative role against renal damage and oxidative stress induced by DIC in male rats.


2020 ◽  
Author(s):  
Gengxiang Wu ◽  
Xue Hu ◽  
Jinli Ding ◽  
Jing Yang

Abstract Background Previous studies have shown that chronic inflammation and oxidative stress may play an important role in the pathophysiology of polycystic ovary syndrome (PCOS), and glutamine (Gln) showed the anti-inflammatory and antioxidant properties. So the aim of this study is to investigate the effect of glutamine supplementation on PCOS rats. Methods Female Sprague–Dawley rats were randomly assigned into five groups (n = 10 /group), control group, PCOS group, PCOS+0.5g/kg Gln group, PCOS+0.75g/kg Gln group and PCOS+1.0g/kg Gln group. All the PCOS rats were administrated with 6 mg/100 g dehydroepiandrosterone (DHEA) for 20 consecutive days, all the PCOS+Gln groups were intraperitoneal injected Gln twice in the next morning after the last DHEA injection. All the samples were collected 12 hours after the last administration. Ovarian histological examinations were analyzed and the concentration of serum hormone, inflammatory and oxidative stress factors were measured. Results There was no obvious ovarian histological change among the PCOS group and PCOS+Gln groups. All the detected inflammation factors (IL-6, IL-18, TNF-α and CRP) showed significantly higher in all the PCOS groups compared to the control group (P<0.01), and were significantly decreased with the low supplementation of glutamine (P<0.01, include 0.5g/kg group and 0.75g/kg group).Concentrations of SOD were significantly lower in all the PCOS groups (P<0.01) compared to the control group, and increased significantly with the low supplementation of glutamine (P<0.01, include 0.5g/kg group and 0.75g/kg group). Serum concentrations of MDA, NO and NOS were significantly higher in PCOS group (P<0.01) compared with the control group, and significantly decreased to the comparative levels of control group with the low supplementation of glutamine (P<0.01, include 0.5g/kg group and 0.75g/kg group). Conclusion There is low-grade inflammation and oxidative stress in DHEA-induced PCOS rats. The supplementation of glutamine with doses of 0.5g/kg and 0.75g/kg could effectively ameliorate the inflammatory and oxidative stress conditions of PCOS.


2021 ◽  
Author(s):  
ZiJing Guo ◽  
ZhiChao Wang ◽  
KeXin Ma ◽  
Baozhu Ding ◽  
GuoPing Ma ◽  
...  

Abstract BackgroundThe main purpose is to establish an ideal arrhythmia model with isoproterenol and explore its mechanism.MethodsFifty healthy male SD rats were randomly divided into the control (CON) group, subcutaneous injection (SC) group(ISO 5 mg/kg for 2 consecutive days), intraperitoneal injection (IP) group (ISO 5 mg/kg for 2 consecutive days), 2+1 group (ISO 5mg/kg by SC for 2 consecutive days, then ISO 3mg /kg by IP for 1 day), 6+1 group ( ISO 5mg/kg by SC for 6 consecutive days, then ISO 3mg /kg by IP for 1 day).The ECG were recorded by BL-420F system. The pathological changes in myocardial tissue were observed by HE and Masson staining. The serum cTnI, TNF-α, IL-6, and IL-1β levels were detected by ELISA. Serum CK, LDH and oxidative stress-related indicators were detected by an automatic biochemical analyser. ResultsThe cardiomyocytes in the CON group rats were normal, while those in the other groups showed signs of disorder, unclear borders, and lysis and necrosis, especially in the 6+1 group. The incidence of arrhythmia, arrhythmia score, and the levels of serum myocardial enzymes, troponin, and some inflammatory factors in the 2+1 group and 6+1 group were higher than those in the single injection way (P<0.01 or P<0.05). The indicators in the 6+1 group were mostly higher than those in the 2+1 group (P<0.01), and the SOD level in the 6+1 group was lower than that in the CON group; the MDA and NO higher(P<0.01 or P<0.05). ConclusionThe combined mode of ISO injection (SC with IP) is more likely to induce arrhythmia than single ISO injection. The "6+1" method of ISO injection can establish a more stable arrhythmia model. Cardiomyocyte damage induced by oxidative stress and inflammation is an important mechanism.


2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
G. H. Ragab ◽  
F. M. Halfaya ◽  
O. M. Ahmed ◽  
W. Abou El-Kheir ◽  
E. A. Mahdi ◽  
...  

Until now, there is no treatment that cause complete cure of the chronic inflammatory and degenerative disease, osteoarthritis (OA). Moreover, the underlying mechanisms of OA development and progress are not fully elucidated, and the present pharmacological treatment alternatives are restricted and associated with adverse side effects. Thus, the present study was conducted to evaluate the role of platelet-rich plasma (PRP) in the remedy of OA in the rat model in terms of inflammation, ankle histopathological alterations, and oxidative stress. OA was induced in male Wistar rats by injection of MIA (2 mg)/50 µL isotonic saline in the right ankle joint for two successive days in each rat. After the 2nd MIA injection, the osteoarthritic rats were allocated into two groups such as the MIA group (group 2) and MIA + PRP group (group 3). The MIA + PRP group was treated with PRP (50 µL) by injection into the ankle joint of the right hind limb of each rat at days 14, 21, and 28 after the 2nd injection of MIA. The same equivalent volume of saline, as a substitute of PRP, was injected into the ankle joint of each rat of the normal control group (group 1) and MIA group (group 2) at the same tested periods. Swelling of joint, bodyweight, total leucocytes count (TLC), and morphological as well as histological changes of ankle joints were evaluated. Serum lipid peroxides (LPO), glutathione (GSH), and glutathione S-transferase (GST) levels were examined as biomarkers of oxidative stress. Serum tumor necrosis factor-α (TNF-α), interleukin-17 (IL-17), and interleukin-4 (IL-4) were investigated by ELISA as biomarkers of inflammation. In addition, magnetic resonance imaging (MRI) was carried out to investigate the soft tissues in joints. The obtained results revealed that PRP reduced LPO and increased GSH and GST levels in osteoarthritic rats. Also, PRP significantly diminished serum TNF-α and IL-17 levels, while it increased IL-4 serum levels in rats with MIA-induced OA. Morphological observations, histological analysis, and MRI revealed a gradual diminishing in joint inflammation and destruction of cartilage in PRP-injected osteoarthritic rats. Based on these results, it can be suggested that PRP has antiarthritic potential in MIA-induced OA, which may be mediated via suppression of inflammation and oxidative stress.


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