Evaluation of anti-inflammatory activity of Justicia secunda Vahl leaf extract using in vitro and in vivo inflammation models

Abstract

Abstract Background Justicia secunda Vahl. is a medicinal plant used in ethnomedical practice as therapy to manage inflammation. Therefore, this study was designed to evaluate the anti-inflammatory activity of methanol extract of J. secunda leaves (MEJSL) using in vitro and in vivo inflammation models. Methods Seventy-percent MEJSL was prepared following standard procedure. In vitro anti-inflammatory assays were performed using heat-induced bovine serum albumin (BSA) denaturation and erythrocyte membrane stabilization assays. Carrageenan and formaldehyde induced inflammation in rat models were used to evaluate the anti-inflammatory activity of MEJSL in vivo. Diclofenac sodium was used as a reference drug. In addition, liver and kidney function assays and hematological analysis were carried out. Results Data revealed that varying concentrations of MEJSL significantly (P < 0.05) inhibited heat-induced BSA denaturation and stabilized erythrocyte membrane against hypotonicity-induced hemolysis when compared with diclofenac sodium in a concentration-dependent manner. In vivo study showed that 10 mg/kg body weight (b.w.) diclofenac sodium, 100 and 300 mg/kg b.w. MEJSL suppressed carrageenan-induced paw edema at the sixth hour by 71.14%, 83.08%, and 89.05%, respectively. Furthermore, 10 mg/kg b.w. diclofenac sodium, 100 and 300 mg/kg b.w. MEJSL inhibited formaldehyde-induced paw edema by 72.53%, 74.73%, and 76.48%, respectively. Animals treated with varying doses of MEJSL had reduced plasma aspartate aminotransferase and alanine aminotransferase activities; urea and creatinine concentrations; and modulated hematological parameters when compared with the untreated control group. Conclusions Findings from this study showed that MEJSL exhibited substantial anti-inflammatory actions in the in vitro and in vivo models. It also indicated that MEJSL anti-inflammatory mechanisms of action could be through interference with phase 2 inflammatory stressors, upregulation of cytoprotective genes, stabilization of inflammatory cell membranes and immunomodulatory activity.