Low quality evidence shows oral and IM vitamin B having similar effects in terms of normalising serum vitamin B levels, but oral treatment costs less. We found very low-quality evidence that oral vitamin B appears as safe as IM vitamin B. Further trials should conduct better randomisation and blinding procedures, recruit more participants, and provide adequate reporting. Future trials should also measure important outcomes such as the clinical signs and symptoms of vitamin B deficiency, health related-quality of life, socioeconomic effects, and report adverse events adequately, preferably in a primary care setting.
The flower of Edgeworthia gardneri (Wall.) Meisn is commonly used in beverage products in Tibet and has potential health benefits for diabetes. However, the mechanisms underlying anti-insulin resistance (IR) action of the flower of E. gardneri are not fully understood. This study aims to investigate the effects of the water extract of the flower of E. gardneri (WEE) on IR in palmitate (PA)-exposed HepG2 hepatocytes. WEE was characterized by UPLC analysis. PA-treated HepG2 cells were selected as the IR cell model. The cell viability was determined using MTT assay. Moreover, the glucose consumption and production were measured by glucose oxidase method. The glucose uptake and glycogen content were determined by the 2-NBDG (2-deoxy-2-[(7-nitro-2,1,3-benzoxadiazol-4-yl) amino]-D-glucose) glucose uptake assay and anthrone-sulfuric acid assay, respectively. The intracellular triglyceride content was detected by oxidative enzymic method. Protein levels were examined by Western blotting. Nuclear localization of FoxO1 was detected using immunofluorescence analyses and Western blotting. The expression of FoxO1 target genes was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The viability of PA-treated HepG2 cells was concentrationdependently increased by incubation with WEE for 24 h. WEE treatment remarkably increased the consumption and uptake of glucose in PA-exposed HepG2 cells. Moreover, treatment with WEE significantly decreased the PA-induced overproduction of glucose in HepG2 cells. After exposure of HepG2 cells with PA and WEE, the glycogen content was significantly elevated. The phosphorylation and total levels of IRb, IRS1, and Akt were upregulated by WEE treatment in PA-exposed HepG2 cells. The phosphorylation of GSK3b was elevated after WEE treatment in PA-treated cells. WEE treatment also concentration-dependently downregulated the phosphorylated CREB, ERK, c-Jun, p38
Aim: To investigate the effect of small interfering RNAs targeting mutant K-ras on the growth of pancreatic carcinoma cell lines in vitro and in vivo.Materials and Methods: We cloned targeting sequence spanning codon 12 of mutant K-ras into the pSilencer-hygro plasmid, yielding two recombinant vectors with one base different. Both human pancreatic carcinoma cell lines were transfected by these two recombinant vectors. The transfected PC-7 cells were injected subcutaneously into nude mice to observe its tumorigenicity. RT-PCR and Western blot analysis were carried out to test the expression of K-ras in all of the transfected cell lines. Growth curves assay were performed to test the abilities of cells proliferation. Anti-K-ras therapy of PC-7 and Panc-1 in subcutaneous mice models were performed by intratumor injection of polyethylenimine/ siRNAs complex.Results: The expressions of K-ras in PC-7 cells and Panc-1 cells were significantly inhibited by corresponding small interfering RNAs. The expression of K-ras was particularly inactivated by siRNA without any base mismatch to its homologous mRNA, while this oncogene with central base mismatch could not be inhibited as effectively as that of the former. The growth of PC-7 cells and Panc-1 cells transfected by corresponding mutant K-ras targeted siRNAs were significantly suppressed when compared with controls (p < 0.05). The transfected PC-7 cells lost tumorigenic ability. Four weeks treatment of Xenograft of pancreatic carcinoma (PC-7 and Panc-1) in nude mice with Polyethylenimin e-encapsulated mutant K-ras targeted siRNAs (20 mg/mouse twice weekly) were effective in reducing tumor growth, when compared with controls (p < 0.05).Conclusion: The central base may play a key role in the process of RNA interference. The mutant point and its vicinity of 19 nucleotides in K-ras may be the effective targeting sequence for RNA interference. Targeting mutant-k-ras therapy of pancreatic carcinoma may be a clinically applicable therapeutic modality.
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