scholarly journals Could the Combination of Two Non-Psychotropic Cannabinoids Counteract Neuroinflammation? Effectiveness of Cannabidiol Associated with Cannabigerol

Medicina ◽  
2019 ◽  
Vol 55 (11) ◽  
pp. 747 ◽  
Author(s):  
Mammana ◽  
Cavalli ◽  
Gugliandolo ◽  
Silvestro ◽  
Pollastro ◽  
...  
Keyword(s):  
Additional Treatment ◽  
Bax Protein ◽  
All Trans Retinoic Acid ◽  
Molecular Events ◽  
Tnf Α ◽  
Potential Therapeutic Application ◽  
Anti Oxidant ◽  
Anti Inflammatory ◽  
Pre Treatment ◽  
Apoptotic Effects

Background and Objectives: Neuroinflammation is associated with many neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). In this study, we investigate the anti-inflammatory, anti-oxidant, and anti-apoptotic properties of two non-psychoactive phytocannabinoids, cannabigerol (CBG) and cannabidiol (CBD). Materials and Methods: The motoneuron-like cell line NSC-34 differentiated by serum deprivation and with the additional treatment of all-trans retinoic acid (RA) is a valid model to investigate molecular events linked to neurodegeneration in ALS. Results: Pre-treatment with CBG (at 2.5 and 5 µM doses) alone and in combination with CBD (at 2.5 and 5 µM doses) was able to reduce neuroinflammation induced by a culture medium of LPS-stimulated macrophages. In particular, the pre-treatment with CBD at a 5 µM dose decreased TNF-α levels and increased IL10 and IL-37 expression. CBG–CBD association at a 5 µM dose also reduced NF-kB nuclear factor activation with low degradation of the inhibitor of kappaB alpha (IkBα). CBG and CBD co-administered at a 5 µM dose decreased iNOS expression and increased Nrf2 levels. Furthermore, the pre-treatment with the association of two non-psychoactive cannabinoids downregulated Bax protein expression and upregulated Bcl-2 expression. Our data show the anti-inflammatory, anti-oxidant, and anti-apoptotic effects PPARγ-mediated. Conclusions: Our results provide preliminary support on the potential therapeutic application of a CBG–CBD combination for further preclinical studies.

Evaluation of Anti-inflammatory and Antioxidant Effects of Sumatriptan on Carbon Tetrachloride-induced Hepatotoxicity in Rats

Drug Research ◽  
2021 ◽  
Author(s):  
Ahmad Reza Dehpour ◽  
Hasan Yousefi-Manesh ◽  
Mohammad Sheibani ◽  
Mohammad Amin Sadeghi ◽  
Sara Hemmati ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Histopathological Examination ◽  
Serum Levels ◽  
Control Group ◽  
Adult Rats ◽  
Toxic Agents ◽  
Tnf Α ◽  
Anti Oxidant ◽  
Anti Inflammatory ◽  
Pre Treatment

AbstractThe liver detoxifies and metabolizes many drugs and xenobiotics which may cause hepatotoxicity due to some toxic agents. Carbon tetrachloride (CCl4) is metabolized in cytochrome P450 and its reactive radical metabolites cause lipid peroxidation, cellular injury, and apoptosis. Sumatriptan (SUM), 5-HT1B/1D receptor agonist, had anti-inflammatory and anti-oxidant effects. In this research the effect of SUM pre-treatment against CCl4-induced hepatotoxicity was examined. Adult rats received SUM (0.1, 0.3 and 1 mg/kg; i.p.) for 3 consecutive days before CCl4 (2 ml/kg; i.p. on the 3rd day). The aminotransferases serum levels, tissue levels of anti-oxidant and pro-inflammatory markers and histopathological examination were evaluated. SUM (0.3 mg/kg) prevented significantly the elevation of aminotransferases versus the control group (CCl4 group) (P<0.0001) and also, reversed meaningfully the changes of the MPO, MDA, SOD and CAT, IL-1β and TNF-α levels. Additionally, CCl4-intoxication resulted to the disruption of lobular and cellular structures and inflammation in histopathological evaluation which is prevented by SUM (0.3 mg/kg). These data revealed that SUM (0.3 mg/kg), but no at doses 0.1 and 1 mg/kg, decreases the hepatotoxicity of induced by CCl4 in rats.

scholarly journals Processed Scutellaria baicalensis Georgi Extract Alleviates LPS-Induced Inflammatory and Oxidative Stress through a Crosstalk between NF-κB and KEAP1/NRF2 Signaling in Macrophage Cells

2021 ◽  
Vol 11 (13) ◽  
pp. 6055
Author(s):  
Akhtar Ali ◽  
En-Hyung Kim ◽  
Jong-Hyun Lee ◽  
Kang-Hyun Leem ◽  
Shin Seong ◽  
...  
Keyword(s):  
Scutellaria Baicalensis ◽  
Raw 264.7 Cells ◽  
Prostaglandin E ◽  
Scutellaria Baicalensis Georgi ◽  
Anticancer Effects ◽  
Tnf Α ◽  
Clinical Benefits ◽  
Anti Oxidant ◽  
Cox 2 ◽  
Anti Inflammatory

Prolonged inflammation results in chronic diseases that can be associated with a range of factors. Medicinal plants and herbs provide synergistic benefits based on the interaction of multiple phytochemicals. The dried root of Scutellaria baicalensis Georgi and its compounds possess anti-inflammatory, anti-oxidative, and anticancer effects. Processing is a traditional method to achieve clinical benefits by improving therapeutic efficacy and lowering toxicity. In this study, we investigated the anti-inflammatory and anti-oxidant effect of processed Scutellaria baicalensis Georgi extract (PSGE) against lipopolysaccharide (LPS) stimulated RAW 264.7 cells. Data using Griess assay and ELISA showed that PSGE decreased nitric oxide and prostaglandin E2 (PGE2) levels against LPS. PSGE treatment up-regulated 15-hydroxyprostaglandin dehydrogenase (PGDH), while cyclooxygenase (COX)-2 and microsomal prostaglandin E synthase (mPGES)-1 expression did not change. Interestingly, PGE2 inhibition was regulated by prostaglandin catabolic enzyme 15-PGDH rather than COX-2/mPGES-1, enzymes essential for PGE2 synthesis. Additionally, PSGE-suppressed LPS-induced IL-6 and TNF-α production through NF-κB signaling. NF-κB release from an inactive complex was inhibited by HO-1 which blocked IκBα phosphorylation. The ROS levels lowered by PSGE were measured with the H2DCFDA probe. PSGE activated NRF2 signaling and increased antioxidant Hmox1, Nqo1, and Txn1 gene expression, while reducing KEAP1 expression. In addition, pharmacological inhibition of HO-1 confirmed that the antioxidant enzyme induction by PSGE was responsible for ROS reduction. In conclusion, PSGE demonstrated anti-inflammatory and anti-oxidant effects due to NRF2/HO-1-mediated NF-κB and ROS inhibition.

scholarly journals Camel Milk Attenuates Rheumatoid Arthritis Via Inhibition of Mitogen Activated Protein Kinase Pathway

2017 ◽  
Vol 43 (2) ◽  
pp. 540-552 ◽  
Author(s):  
Hany H. Arab ◽  
Samir A. Salama ◽  
Tamer M. Abdelghany ◽  
Hany A. Omar ◽  
El-Shaimaa A. Arafa ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Mapk Pathway ◽  
Lipid Peroxide ◽  
Mitogen Activated Protein Kinase ◽  
Camel Milk ◽  
Tnf Α ◽  
Mitogen Activated Protein ◽  
Anti Oxidant ◽  
Cox 2 ◽  
Anti Inflammatory

Background/Aims: Camel milk (CM) has shown beneficial anti-inflammatory actions in several experimental and clinical settings. So far, its effect on rheumatoid arthritis (RA) has not been previously explored. Thus, the current work aimed to evaluate the effects of CM in Adjuvant-induced arthritis and air pouch edema models in rats, which mimic human RA. Methods: CM was administered at 10 ml/kg orally for 3 weeks starting on the day of Freund’s adjuvant paw inoculation. The levels of TNF-α and IL-10 were measured by ELISA while the protein expression of NF-κBp65, COX-2 and iNOS was detected by immunohistochemistry. The expression of MAPK target proteins was assessed by Western blotting. Results: CM attenuated paw edema, arthritic index and gait score along with dorsal pouch inflammatory cell migration. CM lowered the TNF-α and augmented the anti-inflammatory IL-10 levels in sera and exudates of arthritic rats. It also attenuated the expression of activated NF-κBp65, COX-2 and iNOS in the lining of the dorsal pouch. Notably, CM inhibited the MAPK pathway signal transduction via lowering the phosphorylation of p38 MAPK, ERK1/2 and JNK1/2 in rat hind paws. Additionally, CM administration lowered the lipid peroxide and nitric oxide levels and boosted glutathione and total anti-oxidant capacity in sera and exudates of animals. Conclusion: The observed CM downregulation of the arthritic process may support the interest of CM consumption as an adjunct approach for the management of RA.

Abstract 620: Angiotensin AT2 Receptor Exerts an Anti-inflammatory Response in Lipopolysaccharide-activated THP-1 Macrophages

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Isha S Dhande ◽  
Tahir Hussain
Keyword(s):  
Inflammatory Response ◽  
Interleukin 10 ◽  
Receptor Expression ◽  
Human Macrophage ◽  
No Production ◽  
At2 Receptor ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Pre Treatment ◽  
Lps Activation

Macrophages have been shown to be an important contributor to the pathogenesis of hypertension and stroke. The angiotensin AT2 receptor (AT2R), which is expressed in macrophages, is known to promote vasodialation, natriuresis and lower inflammation. The goal of the present study was to explore the anti-inflammatory role of AT2R stimulation in human macrophage-like THP-1 cells activated by lipopolysaccharide (LPS). Phorbol 12-myristate 13-acetate (PMA) differentiated macrophage-like THP-1 cells were treated with AT2R agonist C21 (1 μmol/L) for 30 minutes prior to activation with LPS (1 μg/ml). Media and cells were collected after 24 hours and were analyzed for levels of pro- and anti-inflammatory cytokines and proteins. Pre-treatment with C21 resulted in a 4-fold increase (104.8±6.1 vs 406.7±52.3) in anti-inflammatory interleukin-10 (IL-10) production and a 5-fold decrease (3560±237 vs 588.8±15.94) in pro-inflammatory tumor necrosis factor-α (TNF-α) levels in the media in response to LPS. Predictably, LPS resulted in a 6-fold up-regulation of iNOS expression which was prevented with C21 pre-treatment. A modest decrease in the anti-inflammatory macrophage mannose receptor C type 2 (MRC2) expression was detected with LPS treatment. AT2R agonist pre-treatment, however, increased this receptor expression by ~70% after LPS activation. C21 alone also resulted in a 20% increase in MRC2 expression compared to untreated controls. The anti-inflammatory effect of AT2R activation was abolished in the presence of neutralizing IL-10 antibody (1 μg/ml), indicating a central role for IL-10 in mediating the beneficial response to C21 in LPS activated macrophages. Further, inhibition of nitric oxide (NO) by L-NAME prior to C21 pre-treatment also prevented the decrease in TNF-α and increase in IL-10 in response to AT2R agonist, which suggests that the anti-inflammatory response to C21 may be mediated via increase in NO production prior to LPS activation of macrophages. In conclusion, AT2R stimulation may potentially suppress the inflammatory response of macrophages to LPS by shifting the balance from pro- to anti-inflammatory cytokine production and may prove to be beneficial in the control of the inflammatory component of stroke and hypertension.

Detraction of Diclofenac-Associated Hepatotoxicity by Fresh Beet Root Juice in Male Albino Mice

2021 ◽  
Vol 72 (2) ◽  
pp. 19-26
Author(s):  
Tahani Mohamad Alhazani ◽  
Badr Abdullah Aldahmash ◽  
Doaa Mohamed El-Nagar ◽  
Khalid Elfaki Ibrahim ◽  
Saheed Olaide Anifowose ◽  
...  
Keyword(s):  
Liver Enzymes ◽  
Immunohistochemical Analysis ◽  
Control Group ◽  
Beet Root ◽  
Hepatotoxic Effect ◽  
Anti Oxidant ◽  
Albino Mice ◽  
Anti Inflammatory ◽  
Pre Treatment ◽  
Main Component

The beet root as dietary supplement hepatoprotective ability has gained interest in recent days. The present study was designed to determine the potential hepatoprotective effect of beet root juice as anti-inflammatory and anti-oxidant agent to eliminate the hepatotoxic effect of diclofenac as wide spread analgesic agent. Male albino mice were divided randomly into 4 groups, the 1st group served as control group, the 2nd group received 8 mL/kg of freshly prepared beet root juice, the 3rd group received oral administration 20 mg/kg of diclofenac and the 4th group pre-treated with beet root before one-hour diclofenac administration for 30 days. Biochemical results revealed sharp significant raised levels of liver enzymes level (AST, ALT, ALP and GGT) in the 3rd group that received diclofenac, besides to marked pathological changes manifested by high pathological scoring system such as hepatocytes degeneration, ballooning, infiltration and fibrosis. Immunohistochemical analysis elucidated massive incidence of MDA as an indicator of oxidative stress, moreover great number of neutrophils were seen as main component of inflammation. Whereas, pre-treatment of beet root juice one hour before diclofenac resulted in significant decrease of liver enzymes, clear attenuation of pathological features, decrease of pathological score. A great reduction of MDA in liver tissue and number of neutrophils stained histochemically. It was concluded that beet root juice possessed beneficial hepatoprotective role against diclofenac, as significant anti-oxidant and anti-inflammatory effect.

Beneficial effects of nontoxic ozone on H2O2-induced stress and inflammation

2016 ◽  
Vol 94 (6) ◽  
pp. 577-583 ◽  
Author(s):  
Altug Kucukgul ◽  
Suat Erdogan ◽  
Ramazan Gonenci ◽  
Gonca Ozan
Keyword(s):  
Cell Loss ◽  
Alveolar Cells ◽  
Sod Activity ◽  
Beneficial Effects ◽  
Tnf Α ◽  
Ozone Pretreatment ◽  
Anti Oxidant ◽  
Anti Inflammatory ◽  
Vitro Model

In this study, the anti-oxidant and anti-inflammatory efficacy of ozone oxidative preconditioning (OOP) were investigated on hydrogen peroxide (H2O2)-induced human lung alveolar cells. In MTT and trypan blue viability tests, while 100 μmol/L H2O2caused a 17.3% and 21.9% decrease in the number of living cells, respectively, ozone at 20 μmol/L regenerated cell proliferation and prevented 9.6% and 11.0% of cell loss, respectively. In addition, H2O2decreased the transcription levels of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) 5.43-, 2.89-, and 5.33-fold, respectively, while it increased Bax, NF-κβ, TNF-α, and iNOS expression 1.57-, 1.32-, 1.40-, and 1.41-fold, respectively. Ozone pretreatment, however, increased CAT, GPx, and SOD transcription levels 7.08-, 5.17-, and 6.49-fold and decreased Bax, NF-κβ, TNF-α, and iNOS transcriptions by 1.25-, 0.76-, 3.63-, and 7.91-fold, respectively. Moreover, intracellular glutathione (GSH) level and SOD activity were decreased by 46.2% and 45.0% in the H2O2treatment group, and OOP recovered 58.5% and 20.1% of the decreases caused by H2O2. H2O2also increased nitrite levels 7.84-fold, and OOP reduced this increase by half. Consequently, OOP demonstrated potent anti-oxidant and anti-inflammatory effects on in vitro model of oxidative stress-induced lung injury.

Anti-TNF-α Therapy Exerts Intestinal Anti-inflammatory and Anti-Apoptotic Effects After Massive Bowel Resection in a Rat

2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Igor Sukhotnik ◽  
Yoav Ben-Shahar ◽  
Yulia Pollak ◽  
Shlomi Cohen ◽  
Anat Guz-Mark ◽  
...  
Keyword(s):  
Bowel Resection ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Apoptotic Effects ◽  
Massive Bowel Resection

scholarly journals IL-37 expression improves renal function after ischemia and reperfusion in mice model

2021 ◽  
Vol 9 (4) ◽  
pp. 207-224
Author(s):  
Paloma E Pinto ◽  
◽  
Aloisio M Requião-Moura
Keyword(s):  
Renal Failure ◽  
Inflammatory Response ◽  
Renal Ischemia ◽  
Mice Model ◽  
Leukocyte Accumulation ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Apoptotic Effects ◽  
Hematoxylin Eosin ◽  
Human Cytokine

Renal ischemia is a major problem in the world that lead to renal failure for which no effective treatment is available. Renal ischemia involves a robust inflammatory response, involving up-regulated chemokine expression and leukocyte accumulation, contributes to the mechanism of renal injury and renal failure. IL-37 is a new human cytokine and has an anti-inflammatory function. Currently, it is unknown whether IL-37 suppresses renal inflammatory response to ischemia. We tested the hypothesis that expression of human IL-37 in mouse protects the renal against ischemic injury through suppression of the renal inflammatory response. IL-37 Tg and WT mice were subjected to right renal nephrectomy to induce unilateral model of ischemia the microvascular clamp was positioned around the left renal pedicles. Serum sampling for measurements of TNF-α, IL-1β, Caspase3, MDA, HMGB1, urea and creatinine. Hematoxylin-eosin staining for histological analysis. The resulted data showed that IL-37 has anti-inflammatory effects in renal IRI as evidenced by significant reduction of the inflammatory markers levels TNF-α, IL-1β and HMGB1. IL-37 has potent antioxidant and anti-apoptotic effects with significant reduction in MDA and caspace-3 respectively

scholarly journals Antioxidant and Anti-Inflammatory Potential of Thymoquinone and Lycopene Mitigate the Chlorpyrifos-Induced Toxic Neuropathy

2021 ◽  
Vol 14 (9) ◽  
pp. 940
Author(s):  
Mohamed Aboubakr ◽  
Said M. Elshafae ◽  
Ehab Y. Abdelhiee ◽  
Sabreen E. Fadl ◽  
Ahmed Soliman ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Corn Oil ◽  
Organophosphate Pesticide ◽  
Toxic Neuropathy ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Apoptotic Effects ◽  
Oxidative State ◽  
Necrosis Factor

CPF (chlorpyrifos) is an organophosphate pesticide used in agricultural and veterinary applications. Our experiment aimed to explore the effects of thymoquinone (TQ) and/or lycopene (LP) against CPF-induced neurotoxicity. Wistar rats were categorized into seven groups: first group served as a control (corn oil only); second group, TQ (10 mg/kg); third group, LP (10 mg/kg); fourth group, CPF (10 mg/kg) and deemed as CPF toxic control; fifth group, TQ + CPF; sixth group, (LP + CPF); and seventh group, (TQ + LP + CPF). CPF intoxication inhibited acetylcholinesterase (AchE), decreased glutathione (GSH) content, and increased levels of malondialdehyde (MDA), an oxidative stress biomarker. Furthermore, CPF impaired the activity of antioxidant enzymes including superoxide dismutase (SOD) and catalase (CAT) along with enhancement of the level of inflammatory mediators such as tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β. CPF evoked apoptosis in brain tissue. TQ or LP treatment of CPF-intoxicated rats greatly improved AchE activity, oxidative state, inflammatory responses, and cell death. Co-administration of TQ and LP showed better restoration than their sole treatment. In conclusion, TQ or LP supplementation may alleviate CPF-induced neuronal injury, most likely due to TQ or LPs’ antioxidant, anti-inflammatory, and anti-apoptotic effects.

scholarly journals Protective Effects of Total Saponins of Aralia elata (Miq.) on Endothelial Cell Injury Induced by TNF-α via Modulation of the PI3K/Akt and NF-κB Signalling Pathways

2018 ◽  
Vol 20 (1) ◽  
pp. 36 ◽  
Author(s):  
Ping Zhou ◽  
Weijie Xie ◽  
Yun Luo ◽  
Shan Lu ◽  
Ziru Dai ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Injury ◽  
Inflammatory Responses ◽  
Inflammatory Factors ◽  
Early Event ◽  
Protective Effects ◽  
Bax Protein ◽  
Aralia Elata ◽  
Tnf Α ◽  
Anti Inflammatory

Atherosclerosis is an arterial disease associated with inflammation. Hence, the discovery of novel therapeutic agents for suppressing inflammatory responses is urgent and vital for the treatment of atherosclerosis in cardiovascular diseases. The total saponins of Aralia elata (Miq.) Seem. (TAS) are the main components extracted from the Chinese traditional herb Longya Aralia chinensis L., a folk medicine used in Asian countries for treating numerous diseases, enhancing energy and boosting immunity. However, the protective effects of TAS against inflammation-triggered vascular endothelial dysfunction, a critical early event during the course of atherosclerosis, and the potential mechanisms of this protection have been not demonstrated. Accordingly, the aim of this study was to investigate the anti-inflammatory and anti-apoptotic effects and the protective mechanisms of TAS, and show how TAS ameliorates human umbilical vein endothelial cell (HUVEC) damage caused by tumour necrosis factor-α (TNF-α). The results indicated that TAS exerted cytoprotective effects by inhibiting TNF-α-triggered HUVEC apoptosis, mitochondrial membrane potential depolarisation, and the regulation of inflammatory factors (IL-6, MCP-1, and VCAM-1) while suppressing NF-κB transcription. Furthermore, this phenomenon was related to activation of the phosphoinositide 3-kinase (PI3K)/Akt signalling pathway. Blocking the Akt pathway with LY294002, a PI3K inhibitor, reversed the cytoprotective effect of TAS against TNF-α-induced endothelial cell death. Moreover, LY294002 partially abolished the effects of TAS on the upregulation of the Bcl-2 family of proteins and the downregulation of Bax protein expression. In conclusion, the results of our study suggest that TAS suppresses the inflammation and apoptosis of HUVECs induced by TNF-α and that PI3K/Akt signalling plays a key role in promoting cell survival and anti-inflammatory reactions during this process.

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