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Yogurt powder is fermented milk processed in the form of dry yogurt, and has advantages such as stability, storability, convenience, and portability. China and Vietnam are important export target countries because of the increased demand for dairy products. Therefore, we surveyed dairy product standardization in order to establish an export strategy. Lactic acid bacteria counts are unregulated in Korea and Vietnam. In China, lactic acid bacteria counts are regulated at 1×10(6) colony-forming units (CFU)/mL and detected at 6.24±0.33 Log CFU/mL. All three countries have regulated standards for total bacterial counts. In China, total bacterial counts of milk powder are regulated to n=5, c=2, m=50,000, M=200,000 and detected at 6.02±0.12 Log CFU/mL, exceeding the acceptable level. Lactic acid bacterial counts appeared to exceed total bacterial counts. Coliform group counts, Staphylococcus aureus, Listeria monocytogenes, and Salmonella species were not detected. Acidity is not regulated in Korea and Vietnam. In China, acidity was regulated to over 70°T and detected 352.38±10.24°T. pH is unregulated in all three countries. pH was compared to that of general fermented milk, which is 4.2, and that of the sample was 4.28±0.01. Aflatoxin levels are not regulated in Korea and China. In Vietnam, aflatoxin level is regulated at 0.05 ppb. Therefore, all ingredients of the yogurt powder met the safety standards. This data obtained in this study can be used as the basic data in assessing the export quality of yogurt powder.

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The aim of this study was to estimate the shelf life of butter and cheese products, with shelf life being a guide used to determine the storage period of food before deterioration. Butter and cheese samples stored at 10℃ and 15℃ had a shelf life of 221 d, while those stored at 25℃ and 35℃ had a shelf life of 109 d. Quality changes, including total cell count, coliform counts, Listeria monocytogenes counts, acid value, moisture content, pH, acidity and overall sensory evaluation, were monitored. In order to pass the overall sensory evaluation, a quality score of 5 points on a 9-point scale was required. For other quality criteria, legal quality limits were established based on the "Process Criteria and Ingredient Standard of Livestock Products" by the Animal, Plant and Fisheries Quarantine and Inspection Agency (Republic of Korea). The nonlegal quality limit was estimated by regression analysis between non-quality criteria (y) and overall sensory evaluation (x). The shelf life was estimated based on the number of days that the product passed the quality limit of the quality criteria. The shelf life of samples stored at 10℃, 15℃, 25℃ and 35℃ was 21.94, 17.18, 6.10 and 0.58 mon, respectively, for butter and 10.81, 9.47, 4.64 and 0.20 mon, respectively, for cheese.

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OBJECTIVE: Lactic acid bacteria (LAB) can improve disturbances of indigenous microflora as well as inflammatory bowel diseases (IBD) such as ulcerative colitis and Crohn's disease. We examined the anticolitic effect of Lactobacillus suntoryeus HY7801, which inhibited toll-like receptor (TLR)-4-linked NF-kappaB activation in human embryonic kidney (HEK) cells, in 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitic mice. MATERIALS AND METHODS: We measured the ability of commercial and intestinal LAB to inhibit lipopolysaccharide (LPS)-stimulated, TLR-4-linked NF-kappaB activation in HEK cells, as well as to inhibit colitis outcomes in TNBS-induced colitic mice. We also measured levels of the inflammatory markers, interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, and IL-6, and their transcription factor, NF-kappaB, in intestinal mucosa by enzyme-linked immunosorbent assay and immunoblotting. RESULTS AND DISCUSSION: LAB inhibited TLR-4-linked NF-kappaB activation, and L. suntoryeus HY7801 was the most potent inhibitor. Intrarectal treatment of TNBS in mice caused colon shortening and also increased colonic expression of IL-1beta, IL-6, and TNF-alpha expression. However, oral administration of Lactobacillus HY7801 (100 mg/kg) inhibited colon shortening (p < 0.001) and myeloperoxidase activity in TNBS-induced colitic mice (p < 0.0002) and also decreased colonic expression of IL - 1beta (p < 0.003), IL-6 (p < 0.0001), and TNF-alpha (p < 0.0001). Lactobacillus HY7801 inhibited the NF-kappaB activation and TLR-4 expression induced by TNBS, as well as the expression of cyclooxygenase 2. Lactobacillus HY7801 also reduced the activity of intestinal bacterial glycosaminoglycan degradation and beta-glucuronidase induced by TNBS. CONCLUSION: L. suntoryeus HY7801 can improve colitis via the inhibition of TLR-4-linked NF-kappaB activation.

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An herbal extract mixture and yogurt added to the herbal extract mixture were tested for their protective and therapeutic effects on ethanol-induced liver injury. The herbal extract mixture, yogurt and commercial drugs were used for treatment for two weeks prior to administering a single oral dose of ethanol (3 g/kg body weight). The herbal extract mixture and yogurt added to the herbal extract mixture were found to provide protection against ethanol-induced toxicity comparable to the commercial drug treatment, according to the serum and histopathological analysis. It was also shown that co-treatment with herbal extract mixture and yogurt against a triple oral dose of ethanol (2 g/kg body weight, over one week) provided protection against ethanol toxicity. After the initial set of experiments, the herbal extract mixture and yogurt treatments were extended for three more weeks. When compared to the positive control, further treatment with both the herbal extract and yogurt significantly reduced liver injury and resulted in a lower grade of lipid deposition.

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The hepatoprotective activity of lactic acid bacteria (Lactobacillus brevis HY7401, Lactobacillus acidophilus CSG and Bifidobacterium longum HY8001), which inhibited beta-glucuronidase productivity of intestinal microflora, on t-BHP- or CCl4-induced hepatotoxicity of mice were evaluated. These oral administration of lactic acid bacteria lowered beta-glucuronidase production of intestinal microflora as well as Escherichia coli HGU-3. When lactic acid bacteria at a dose of 0.5 or 2 g (wet weight)/kg was orally administered on CCl4-induced liver injury in mice, these bacteria significantly inhibited the increase of plasma alanine transferase and aspartate transferase activities by 17-57% and 57-66% of the CCl4 control group, respectively. These lactic acid bacteria also showed the potent hepatoprotective effect against t-BHP-induced liver injury in mice. The inhibitory effects of these lactic acid bacteria were more potent than that of dimethyl diphenyl bicarboxylate (DDB), which have been used as a commercial hepatoprotective agent. Among these lactic acid bacteria, L. acidophilus CSG exhibited the most potent hepatoprotective effect. Based on these findings, we insist that an inhibitor of beta-glucuronidase production in intestine, such as lactic acid bacteria, may be hepatoprotective.

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