Volume 29, Issue 5 (8-2022)
RJMS 2022, 29(5): 172-181 |
Back to browse issues page
Research code: 0
Ethics code: 0
Clinical trials code: 0
Department of Cardiovascular Medicine, Shiraz University of Medical Sciences, Shiraz, Iran , MD_parizi@yahoo.com
Abstract: (211 Views)
Background & Aims: To date, much has been reported about the cardiovascular toxicity of NSAIDs, and often conflicting results have been obtained, particularly for aspirin and naproxen, as well as similar results for patients taking ibuprofen. To date, clinical research on the effect of NSAIDs in cardiovascular patients has been limited to pilot studies of flurbiprofen, meloxicam, and parecoxib/valdecoxib. The mechanism of cardiovascular action of aspirin, naproxen, and other non-selective NSAIDs and COX-2 inhibitors is still debated. Although non-selective NSAIDs inhibit both COX-1 and COX-2 enzymes, selective COX-2 inhibitors, including lumiracoxib, have no effect on COX-1 at therapeutic concentrations. The primary hypothesis explaining the increased risk of cardiovascular disease with COX-2 inhibitors is that the inhibitor of this enzyme causes an imbalance and consequently the accumulation of platelets due to COX-1, while the production of COX-2-dependent prostacyclin is inhibited by endothelial cells, which can act on blood vessels. Inhibition of COX by NSAIDs leads to a reduction in the systemic vasodilation effect of prostaglandins such as PG I2, PG E2, and group (CINOD), which are prescribed for the treatment of patients with OA and are more useful in order to reduce CVD complications compared to NSAIDs. A lot of clinical and experimental evidence shows that NSAIDs and COX-2 inhibitors may cause vasoconstriction. Considering the tendency of people to use herbal medicines and also in order to reduce the cardiovascular side effects of chemical drugs for the treatment of OA, it seems necessary to use alternative methods, including the use of medicinal plants, among these plants is wild anemone. This study examines the effect of inflammation in MIA-induced osteoarthritis on physiological cardiovascular performance in male rats with two hypotheses to confirm osteoarthritis and the effective dose of injectable and oral wild anemone extract and the cardiovascular effect of the effective dose of injectable wild anemone extract.
Methods: The data were analyzed using SPSS software and using the Independent T-test to check the differences between groups and the Paired sample T-test to check the differences between the different stages of a group, considering p<0.05. The significance level title was analyzed.
Results: Osteoarthritis (OA) is the most common joint disease in adults worldwide, and knee osteoarthritis is the most common type. The most common symptom of osteoarthritis is joint pain. Osteoarthritis is a common degenerative joint cartilage disorder, with hypertrophic changes in the subchondral bone, which causes inflammation of the surrounding tissues.
Conclusion: The results of this research showed that wild anemone extract can significantly inhibit the process of OA in rats suffering from arthritis with monosodium iodoacetate (especially at a dose of 200 mg/kg) and reduce the edema and weight of the affected rats with consumption. The oral extract of wild anemone showed that anthocyanin (an active substance in wild anemone) had an anti-inflammatory effect through the mechanism of inhibiting the activity of inflammatory cells and pro-inflammatory cytokines in monosodium iodoacetate model mice. Also, the decrease in the level of the creatine kinase-MB enzyme in the coronary fluid in the group receiving wild anemone confirms the fact that the presence of anthocyanin can reduce the risk of CVD and cause endothelial dysplasia by increasing the phosphorylation of protein kinase C hypertrophy and the activation of protein kinase B Akt It improves vascular stiffness, which has a protective effect on the heart. And since the wild anemone was used in this study, according to previous studies, it has been shown that it caused a significant decrease in the proliferation of monkey kidney cancer cells (IC50 = 7.80 μg/ml) and the inhibitory effect of the extract on DPPH radical (74/ 5 μg/ml) also reported that the extract had a phenolic content more than the flavonoid content, which makes its use relatively safe. On the other hand, the increase in blood pressure (mean arterial pressure, systolic and diastolic pressure) can be related to the activity of the vagus nerve, which causes There is a significant decrease in the heart rate and contraction power of the heart. Also, in the serological findings of the present study, it has been shown that the level of troponin has decreased with the consumption of wild anemones. On the other hand, acetylcholine released from nerve endings through M2 muscarinic receptors causes the opening of a group of potassium channels and increases potassium release and hyperpolarization of action potential generating nodes in the heart. Also, nicotinic receptor (α7(α7nAChR) is present in synovial tissue. This has been shown for the synovial tissue of the knee joint of patients with OA, which can produce local acetylcholine in joint inflammation, which is attributed to the cholinergic system. Which inhibits the production of inflammatory cytokines. Also, stimulation of articular chondrocytes by IL-1β or TNF-α for p65 NF-κB nuclear transfer involves a wide range of catabolic genes such as nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in chondrocytes, which leads to the production of proteases. It destroys and weakens the extracellular matrix. Wild anemone decreased TNF-α in the rat knee joint, which is in line with the study. On the other hand, it has been shown in epidemiological studies that there is a relationship between the increase in the level of inflammatory markers and the high prevalence of CVD. Studies have shown that systemic and chronic inflammation can increase the risk of cardiovascular diseases. Since synovial inflammation plays a role in the early stages of OA, CVD is one of the side effects of OA. OA is associated with mild to moderate pain symptoms, and the first line of treatment for this disease is the use of non-steroidal anti-inflammatory drugs (NSAIDs) such as celecoxib. However, the dangerous side effects of NSAIDs in the occurrence of cardiovascular disease in these people limit the long-term use of NSAIDs. Using alternative methods, including the use of medicinal plants, can prevent side effects. Among these plants is the wild anemone with the scientific name (Papaver rhoeas L.), which has anti-inflammatory properties and is effective in spasms.
Methods: The data were analyzed using SPSS software and using the Independent T-test to check the differences between groups and the Paired sample T-test to check the differences between the different stages of a group, considering p<0.05. The significance level title was analyzed.
Results: Osteoarthritis (OA) is the most common joint disease in adults worldwide, and knee osteoarthritis is the most common type. The most common symptom of osteoarthritis is joint pain. Osteoarthritis is a common degenerative joint cartilage disorder, with hypertrophic changes in the subchondral bone, which causes inflammation of the surrounding tissues.
Conclusion: The results of this research showed that wild anemone extract can significantly inhibit the process of OA in rats suffering from arthritis with monosodium iodoacetate (especially at a dose of 200 mg/kg) and reduce the edema and weight of the affected rats with consumption. The oral extract of wild anemone showed that anthocyanin (an active substance in wild anemone) had an anti-inflammatory effect through the mechanism of inhibiting the activity of inflammatory cells and pro-inflammatory cytokines in monosodium iodoacetate model mice. Also, the decrease in the level of the creatine kinase-MB enzyme in the coronary fluid in the group receiving wild anemone confirms the fact that the presence of anthocyanin can reduce the risk of CVD and cause endothelial dysplasia by increasing the phosphorylation of protein kinase C hypertrophy and the activation of protein kinase B Akt It improves vascular stiffness, which has a protective effect on the heart. And since the wild anemone was used in this study, according to previous studies, it has been shown that it caused a significant decrease in the proliferation of monkey kidney cancer cells (IC50 = 7.80 μg/ml) and the inhibitory effect of the extract on DPPH radical (74/ 5 μg/ml) also reported that the extract had a phenolic content more than the flavonoid content, which makes its use relatively safe. On the other hand, the increase in blood pressure (mean arterial pressure, systolic and diastolic pressure) can be related to the activity of the vagus nerve, which causes There is a significant decrease in the heart rate and contraction power of the heart. Also, in the serological findings of the present study, it has been shown that the level of troponin has decreased with the consumption of wild anemones. On the other hand, acetylcholine released from nerve endings through M2 muscarinic receptors causes the opening of a group of potassium channels and increases potassium release and hyperpolarization of action potential generating nodes in the heart. Also, nicotinic receptor (α7(α7nAChR) is present in synovial tissue. This has been shown for the synovial tissue of the knee joint of patients with OA, which can produce local acetylcholine in joint inflammation, which is attributed to the cholinergic system. Which inhibits the production of inflammatory cytokines. Also, stimulation of articular chondrocytes by IL-1β or TNF-α for p65 NF-κB nuclear transfer involves a wide range of catabolic genes such as nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in chondrocytes, which leads to the production of proteases. It destroys and weakens the extracellular matrix. Wild anemone decreased TNF-α in the rat knee joint, which is in line with the study. On the other hand, it has been shown in epidemiological studies that there is a relationship between the increase in the level of inflammatory markers and the high prevalence of CVD. Studies have shown that systemic and chronic inflammation can increase the risk of cardiovascular diseases. Since synovial inflammation plays a role in the early stages of OA, CVD is one of the side effects of OA. OA is associated with mild to moderate pain symptoms, and the first line of treatment for this disease is the use of non-steroidal anti-inflammatory drugs (NSAIDs) such as celecoxib. However, the dangerous side effects of NSAIDs in the occurrence of cardiovascular disease in these people limit the long-term use of NSAIDs. Using alternative methods, including the use of medicinal plants, can prevent side effects. Among these plants is the wild anemone with the scientific name (Papaver rhoeas L.), which has anti-inflammatory properties and is effective in spasms.
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |