Effect of SKB-Gutbiotic on acetic acid induced ulcerative colitis in male Wistar rats

Inflammatory bowel disease (IBD) is a chronic intestinal inflammation gaining increasing attention as it affects considerable number of humans. IBD is reported as ulcerative colitis (UC) and Crohn's disease (CD) Conventional therapies currently available are not satisfactory. Therefore, here, we investigated the effect of SKB-Gutbiotic on acetic acid induced ulcerative coltis (UC) in male Wistar rats. Male Wistar rats, 200-250 g were divided into six groups as follows: Gr. I (control) received 10 mL/kg of distilled water for 21 consecutive days. Gr. II received 2 mL of 4% acetic acid solution once intra rectally for induction of colitis. Gr. III received 2 mg/kg prednisolone as standard control. Groups IV, V & VI were treated with SKB-Gutbiotic @2×109, 20×109 and 50×109 Cfu/kg, respectively. All the animals from each group were sacrificed 24 h after the induction of colitis. Disease activity index, macroscopical damage, hematological parameters, level of superoxide dismutase (SOD), myeloperoxidase (MPO), reduced glutathione (GSH) and histopathological alterations were evaluated. Acetic acid-induced colitis significantly caused alteration in disease activity index, macroscopical damage, MPO and GSH levels (P <0.05) as compared to control group. SKB-Gutbiotic (20×109 and 50×109 Cfu/kg) administration significantly decreased disease activity index, MPO, SOD, increased GSH levels (P <0.05) as compared to colitis rats. In conclusion, SKB-Gutbiotic (20×109 and 50×109 Cfu/kg) significantly showed protective effects against acetic acid-induced colitis as a consequence of its anti-inflammatory and antioxidative properties.

Effect of ethanolic extract of Coriandrum sativum L. on tacrine induced orofacial dyskinesia.

The effect of ethanolic extract of Coriandrum sativum L. seeds (100, 200 mg/kg) was studied on tacrine induced orofacial dyskinesia. Tacrine (2.5 mg/kg, i.p.) treated animals were observed for vacuous chewing movements (VCM), tongue protrusions (TP) and orofacial bursts (OB) for 1 h followed by observations for locomotor changes and cognitive dysfunction. Sub-chronic administration of Coriandrum sativum L. seed extract (E-CS) (100, 200 mg/kg, p.o., for 15 days significantly (P <0.05) decreased the tacrine induced VCM, TP and OB; and also significantly (P <0.05), increased locomotion and cognition compared to the tacrine treated group. Biochemical analysis revealed that tacrine administration significantly (P <0.05) decreased the levels of superoxide dismutase (SOD), Catalase (CAT), glutathione reductase (GSH) levels and also significantly (P <0.05) increased lipid peroxidation (LPO) as an index of oxidative stress, whereas sub-chronic administration of E-CS significantly (P <0.05) improved the antioxidant enzyme (i.e. SOD, CAT, and GSH) levels and also significantly (P <0.05) decreased lipid peroxidation (LPO). The results have demonstrated the protective role of ethanolic extract of Coriandrum sativum. L against tacrine induced orofacial dyskinesia.

Intravenous human umbilical cord blood improves elctrophysiological and metabolic properties in ISO induced myocardial necrosis in rats.

Rats treated with isoproterenol (ISO, 85 mg/kg, sc, twice at an interval of 24 h) showed a significant increase in heart rate, mean arterial blood pressure, pressure rate index, ST elevation on ECG, and a significant increase in the levels of cardiac marker enzymes- lactate dehydrogenase, and creatine kinase in serum and a significant reduction in superoxide dismutase, and catalase and increase in thiobarbituric acid reactive substance activity in heart tissue. Treatment with Human umbilical cord blood (hUCBC; 500 and 1000 µL, iv, via the tail vein; 2 h after the second dose of ISO) significantly restored back to normal levels and showed a lesser degree of cellular infiltration and infarct size in histopathological and planimetry studies respectively. Thus, hUCBC ameliorates cardiotoxic effects of isoproterenol and may be of value in the treatment of myocardial infarction.