Synthesis And Evaluation Of Phthalate Analogue Of Diclofenac Against Freund’s Complete Adjuvant Induced Arthritis In Rat

Objective: The objective of the present study is to evaluate the effect of Phthalate analogues of diclofenac in Freund’s complete adjuvant (FCA) induced Arthritis in the rat. Methods: Twenty four female albino wistar rats were enrolled in this study and are divided into 4 groups (six each). The groups were designed as follows: Group I: vehicle control, Group II: arthritic control, Group III: diclofenac treated, Group IV: phthalate analogue of diclofenac treated. Various assessments such as anti-arthritic activity, biochemical estimations, haematological parameters, ulcerogenesis, radiological and histopathological studies were evaluated. Results: Arthritic control group exhibited significant increase in the level of paw volume, arthritic score (p<0.0001), Serum glutamic pyruvic transaminase (SGPT) (p<0.001), Serum glutamic oxaloacetic transaminase (SGOT) p<0.01), rheumatoid arthritis factor, C-reactive protein (CRP), White Blood Cells (WBC), Creatinine and uric acid and a significant decrease in Red Blood Cells (RBC). Increased swelling of joints, bony destruction and profound ulceration were observed in the Arthritic control group. All these conditions were reversed in diclofenac and phthalate analogue of diclofenac groups. Conclusion: We conclude that phthalate analogue of diclofenac shows potent anti-arthritic activity with milder ulceration when compared to diclofenac treatment.

Antiarthritic activity of Cynodon dactylon (L.) Pers.

Cynodon dactylon (L.) (Poaceae) is traditionally used herb to treat fevers, skin diseases and rheumatic affections. The ethanolic extract of C. dactylon was found to be safe at all the dose levels (100, 200 and 400 mg/kg, orally) and there was no mortality up to the dose of 5000 mg/kg of extract when administered orally. C. dactylon showed significant antiarthritic activity against Freund’s complete adjuvant induced arthritis in rats. Treatment with C. dactylon significantly reduced the mean percentage change in injected and non injected paw, ankle diameter, clinical severity and significantly increased body weight. Results were confirmed using biochemical parameters; there was a significant improvement in the levels of Hb and RBC in C. dactylon treated rats. The increased levels of WBC, ESR, C- reactive protein (CRP) and TNFα were significantly suppressed in C. dactylon treated rats. C. dactylon showed protective effect in arthritic joints but it has been supported by an improvement in bone lesions rather than in cartilage lesions. It can be concluded that ethanolic extract of C. dactylon at a dose of 400 mg/kg is effective in improving haematological level, CRP and reducing TNFα level. Phytochemical screening showed the presence of alkaloids, flavonoids and glycosides in ethanolic extract. All the above results support the traditional uses of the plant in the treatment of rheumatoid arthritis.

Usos y efectos del fosfato de calcio amorfo (FCA) en la odontología restauradora y preventiva / Uses and effects of amorphous calcium phosphate (FCA) in preventive and restorative dentistry

En el presente trabajo se realizó una revisión de la literatura, con el fin de compartir con el gremio odontológico, la información recolectada sobre los usos y efectos actualizados del Fosfato de Calcio Amorfo (FCA) en la odontología, material que promete ser una importante contribución para la protección del medio oral, en un amplio número de situaciones, en las que pueda haber un desequilibrio mineral

This paper reports a literature review which shares the gathered information with the Dental community about the innovate uses and effects of the Amorphous Calcium Phosphate (ACP) with the dentistry, this material will be a significant contribution to the oral environment protection, in lots of situations that could has a mineral unbalance

Effect of Administering Freund's Complete Adjuvant to Spinal Nerves on the Development of Allodynia in the Rat / 대한마취과학회지

BACKGROUND: Spinal nerve ligation injury causes a neuropathic pain syndrome that includes allodynia. Neuropathic pain is also induced by Freund's complete adjuvant (FCA)-induced inflammation. This study was designed to examine the development of mechanical and cold allodynia after FCA administration at the L4/L5 spinal nerves and to compare it with the effects of spinal nerve ligation at the same site. METHODS: Rats were randomly allocated into three groups: (i) treatment with tight ligation of the left L5/L6 spinal nerves, (ii) wrapping of the L5/L6 spinal nerves with Spongostan(R) soaked in FCA, or (iii) wrapping of the L5/L6 spinal nerves with Spongostan(R) soaked in saline. Mechanical and cold allodynia were measured by applying von Frey filaments or acetone in both hind paws. To examine the development of allodynia, the frequencies of hind paw withdrawal to each type of stimulus were measured. RESULTS: Both FCA administration and nerve ligation injury caused a marked mechanical and cold allodynia in the lesioned hind paw compared to saline treatment (P < 0.05). Furthermore, the frequencies of response of the lesioned hind paw to both types of stimulus were significantly greater than those on the contralateral side. CONCLUSIONS: These results suggest that administration of FCA to the spinal nerves can produce a mechanical and cold allodynia with a similar profile of pain facilitation as nerve ligation.

Comparison of the Antiallodynic Effects of Intrathecal Lidocaine and MK-801 on Mechanical Allodynia in Two Neuropathic Pain Rat Models / 대한마취과학회지

BACKGROUND: Neuropathic pain can be induced by nerve injury or inflammation. An N-methyl-D-Aspartate (NMDA) antagonist (MK-801), and a sodium channel blocker (lidocaine) have been found to reduce mechanical allodynia. This study was conducted to determine whether intrathecal lidocaine or MK-801 had an antiallodynic effect on established mechanical allodynia in two well-characterized neuropathic pain rat models. METHODS: Male Sprague Dawley rats (n = 107) were anesthetized, and the left L5 and L6 spinal nerves were ligated (SNL group) or Freund complete adjuvant (FCA) was administrated to the same spinal nerves (FCA group) in order to cause neuropathic pain. A catheter was then implanted into the lumbar intrathecal space. After obtaining the baseline scores, time-effect curves of each drug were established for the antiallodynic effects of lidocaine (30g, 100g and 300g) and MK-801 (1g, 3g, 10g and 30g). The allodynic thresholds for the left hind paw withdrawal to von Frey hairs were assessed and converted to %MPE, and the ED50 value was then calculated using the %MPE. The antiallodynic effects of the two groups were then compared by analyzing the dose-response curves and the ED50 values. RESULTS: Both intrathecal lidocaine and MK-801 resulted in a dose dependent antiallodynic effect. ED50 values and the analysis of dose response curves showed that intrathecal lidocaine provided more effective antiallodynia in the SNL group, whereas intrathecal MK-801 resulted in a greater antiallodynic effect in the FCA group. CONCLUSIONS: In the SNL group, lidocaine had a better effect in reducing allodynic pain, whereas in the FCA group, MK-801 showed a greater antiallodynic effect.

The Expression and Function of Fca Receptor on Human Airway Smooth Muscle Cells / 医学研究杂志

Objective To investigate the expression and function of Fca receptor on human airway smooth muscle(ASM)cells.Methods RT-PCR and immunofluorescence technique were used to detect the expression of Fca receptor on human ASM cells.The effect of IgA on intracellular calcium concentration of human ASM cells was measured by using Fura-2/AM as a calcium indicator.Results RT-PCR and immunofluorescence staining confirmed the presence of Fca receptor on human ASM cells.Compared with control,secretory IgA(sIgA)induced a rise in intracellular calcium concentrations on human ASM cells after 90min incubation(P0.05).Conclusion Fca receptor was expressed on human ASM cells.SIgA increased the intracellular calcium concentration of human ASM cells.

Effect of Nitric Oxide on the Change of Spinal Neuropeptide in the Inflammation Model by Freund's Complete Adjuvant / 대한해부학회지

Injection of Freund's complete adjuvant (FCA) into the plantar surface of the rat induces inflammatory responses with accompanying pain behaviors. Signs of pain behaviors observed in FCA-injected animals are reported to be similar to symptoms seen in patients with inflammatory pain. In the previous study, injection of FCA produced a significant mechanical allodynia over time. The role of substance-P and calcitonin gene-related peptide(CGRP) on allodynia induced by inflammation is still controversial. We investigated the change of spinal neuropeptides and nitric oxide (NO) in rats with inflammation induced by subcutaneous injection of FCA into hind paw. The results are: 1. The number of NADPH-diaphorase and substance P positive neurons increased at ipsilateral spinal ventral horn after FCA injection. No significant changes were found with L-NAME posttreatment. 2. Staining intensity of substance P-immunoreactive area increased at ipsilateral spinal dorsal horn after FCA injection. No significant changes were found with L-NAME posttreatment. 3. CGRP immunoreactivity changed in the same pattern with substance P in all group. The results suggest that spinal neuropeptide substance P and CGRP are involved in the mechanism of the development and maintenance of allodynia in a state of FCA-induced inflammaion. NO may be also involved in the regulation of the quantity of substance P and CGRP in spinal cord.

Effect of Nitric Oxide on Neuropeptide Y Immunoreactivity in Rat Spinal Cord on the Allodynia of Inflammation Induced by Freund's Complete Adjuvant / 대한해부학회지

Injection of Freund's complete adjuvant (FCA) into peripheral tissue induces inflammatory responses with accompanying pain behaviors. Injection of FCA produced a significant mechanical allodynia over time and nitric oxide(NO) is involved in this mechanism. The role of neuropeptide Y (NPY) on allodynia induced by inflammation is still controversal. We invastigated the change of spinal NPY and nitric oxide in rats with inflammation induced by subcutaneous injection of FCA and L-NG-nitro arginine methyl ester (L-NAME) into hind paw. The results are: The number of NADPH-diaphorase positive neurons and staining intensity of area increased at ipsilateral spinal ventral/dorsal horn of inflammation model. No significant changes were found with L-NAME posttreatment. Staining intensity of NPY immunoreactive (ir) area increased at ipsilateral spinal dorsal horn after FCA injection. No significant changes were found with L-NAME posttreatment. NPY-ir and NADPH-d reactive neurons were found in Rexed III-IV lamina at spinal dorsal horn. No significant change were found on all groups. The results suggest that spinal NPY is involved in the mechanism of the development and maintenance of allodynia in a state of FCA-induced inflammaion. NO may be also involved in the regulation of the quantity of NPY in spinal cord level.

A change of nitric oxide in rat DRG following Freund's Complete Adjuvant induced inflammtory pain / 대한해부학회지

It has been reported that injection of Freund's complete adjuvant (FCA) into the hindpaw of a rat induces inflammatory responses with accompanying pain behaviors. Signs of pain behaviors observed in FCA-injected animals were reported to be similar to symptoms seen in patients with inflammatory pain. The nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) is a selective histochemical marker for the nitric oxide synthesizing enzyme, nitric oxide synthase (NOS). N (G)-nitro-L-arginine methyl ester (L-NAME) is a NOS inhibitor. In the present study, we examined if inflammaory pain causes increases in NADPH-diaphorase reactivities in neurons of the dorsal root ganglia (DRG). The results were as follows; 1. FCA-induced inflammation on a limb increased staining density (SD) of NADPH-d positive neurons in the ipsilateral side DRG. 2. Pretreatment of L-NAME did not changed SD of NADPH-d positive neurons on the inflammation of contralateral side DRG 3. Posttreatment of L-NAME decreased the inflammation induced SD of NADPH-d positive neurons. 4. n-NOS immunoreactivity did not match NADPH-d histochemical study, implying the constant level of enzyme itself. Inflammation pain on a hindlimb increased staining density of NADPH-diaphorase positive neuron in the DRG, which was decreased by L-NAME. L-NAME also decreased pain perception. This suggests a role of NO in the pain perception and/or modulation at the level of DRG.