Abstract This study investigated the effect of Lactobacillus isolated from Chinese fermented food on antibiotic-induced intestinal microflora disorder during the early life of mice. The experimental strain Lactobacillus fermentum (LF) CQPC04 was isolated from naturally fermented pickles in Chongqing, China. Lactobacillus plantarum (LP) KFY02 was isolated from naturally fermented yogurt from Korla in the Xinjiang Uygur Autonomous Region. The results showed that LF-CQPC04 and LP-KFY02 alleviated the decrease in bacterial diversity caused by the antibiotics, maintained the abundance of beneficial bacteria, and reduced the abundance of harmful bacteria. These results suggest that LF-CQPC04 and LP-KFY02 can be used as probiotics to alleviate antibiotic-induced intestinal microfloral disorder. antibioticinduced antibiotic induced mice LF (LF CQPC CQPC0 Chongqing China LP (LP KFY KFY0 Region LFCQPC04 LFCQPC LF-CQPC0 LPKFY02 LPKFY LP-KFY0 antibiotics bacteria LFCQPC0 LF-CQPC LPKFY0 LP-KFY

Abstract Purpose Patients with diabetes are vulnerable to myocardial I/R (ischaemia/reperfusion) injury, but are not responsive to IPO (ischaemic post-conditioning). We hypothesized that decreased cardiac Adiponectin (APN) is responsible for the loss of diabetic heart sensitivity to IPO cardioprotecton. Methods Diabetic rats were subjected to I/R injury (30 min of LAD occlusion followed by 120 min of reperfusion). Myocardial infarct area was determined by TTC staining. Cardiac function was monitored by a microcatheter. ANP, 15-F2t-isoprostane, nitrotyrosine and MDA were measured by assay kits. Levels of p-Akt, total-Akt and GAPDH were determined by Western Blot. Results Diabetic rats subjected to myocardial IR exhibited severe myocardial infarction and oxidative stress injury, lower APN in the plasma and cardiac p-Akt expression ( P <0.05). IPO significantly attenuated myocardial injury and up-regulated plasma APN content and cardiac p-Akt expression in non-diabetic rats but not in diabetic rats. Linear correlation analysis showed that the expression of adiponectin was positively correlated with p-Akt and negatively correlated with myocardial infarction area ( P <0.01). Conclusion Protective effect of IPO was tightly correlated with the expression of adiponectin, exacerbation of I/R injury and ineffectiveness of IPO was partially due to the decline of adiponectin and inactivation of Akt in diabetes mellitus.