RESUMO
BACKGROUND: Current therapies are quite unsuccessful in the management of neuropathic pain. Therefore, considering the inhibitory characteristics of GABA mediators, the present systematic review and meta-analysis aimed to determine the efficacy of GABAergic neural precursor cells on neuropathic pain management. METHODS: Search was conducted on Medline, Embase, Scopus, and Web of Science databases. A search strategy was designed based on the keywords related to GABAergic cells combined with neuropathic pain. The outcomes were allodynia and hyperalgesia. The results were reported as a pooled standardized mean difference (SMD) with a 95% confidence interval (95% CI). RESULTS: Data of 13 studies were analyzed in the present meta-analysis. The results showed that administration of GABAergic cells improved allodynia (SMD = 1.79; 95% CI: 0.87, 271; P < 0.001) and hyperalgesia (SMD = 1.29; 95% CI: 0.26, 2.32; P = 0.019). Moreover, the analyses demonstrated that the efficacy of GABAergic cells in the management of allodynia and hyperalgesia is only observed in rats. Also, only genetically modified cells are effective in improving both of allodynia, and hyperalgesia. CONCLUSIONS: A moderate level of pre-clinical evidence showed that transplantation of genetically-modified GABAergic cells is effective in the management of neuropathic pain. However, it seems that the transplantation efficacy of these cells is only statistically significant in improving pain symptoms in rats. Hence, caution should be exercised regarding the generalizability and the translation of the findings from rats and mice studies to large animal studies and clinical trials.
RESUMO
SCOPE: Existing research indicates that anti-inflammatory and antioxidant properties of berberine play major roles in coping with oxidative stress in neurodegenerative diseases, but it is not known if this isoquinoline alkaloid affects inflammatory cytokines such as interleukin 10 in focal cerebral ischemia. METHODS AND RESULTS: Male Wistar rats (10 weeks old) were treated with 40mg/kg concentration of berberine 1h after focal cerebral ischemia and the anti-inflammatory properties of berberine were evaluated by immunohistochemical analysis, water content measure and behavioral tests. Evaluation of infarct volume was performed by TTC staining. Immunohistochemistry and behavioral assessment indicated recovery in treatment group compared to only ischemia group. The infarct volume decreased in treatment group compared to ischemia group. Berberine administration significantly decreased brain edema and contributed to the restoration of motor function. Moreover, berberine potently contributed to neuroprotection in motor area through downregulation of pro-inflammatory cytokines and upregulation of anti-inflammatory cytokines. CONCLUSIONS: These findings confirm the validity of berberine as a potent anti-inflammatory agent in treatment of ischemic stroke.
