OBJECTIVE: This study investigated the potential of Stingless Bee Honey (SBH) to suppress lipopolysaccharide (LPS)-induced systemic acute inflammation in rats and to reveal the probable mechanism of action.
METHODS: Rats received 4.6 and 9.2 g/kg SBH for 7 days followed by a single injection of LPS after which blood samples were taken 6h later.
RESULTS: LPS induced liver, kidney, heart, and lung injury, were manifested by increased serum transaminases, alkaline phosphatase, creatine kinase, creatinine, and urea, along with multiple histological alterations, particularly leukocyte infiltration. Pro-inflammatory cytokines were elevated in the serum, and NF-κB p65, p38 MAPK, and HMGB-1 were significantly increased in different tissues of LPS-challenged rats. SBH prevented tissue injury, ameliorated pro-inflammatory cytokines, and suppressed NF-κB p65, p38 MAPK, and HMGB-1 in rats that had received LPS. In addition, SBH diminished reactive oxygen species (ROS) production, lipid peroxidation, and oxidative DNA damage, and enhanced glutathione and Nrf2 in LPS-treated rats.
CONCLUSION: SBH prevents systemic acute inflammation by suppressing NF-κB, p38 MAPK, HMGB-1, oxidative stress, and tissue injury in rats. Thus, SBH may represent an effective anti-inflammatory nutraceutical, pending further mechanistic studies.
MATERIALS AND METHODS: A retrospective search was carried out on all patients with a diagnosis of achalasia cardia in Hospital Tuanku Ja'afar (HTJ), Seremban, Malaysia between 2014 and 2018. Demographic data, patient symptomatology, and definitive management options were determined from the records. Telephone interviews were conducted to evaluate patient satisfaction with the outcome of treatment.
RESULTS: There were 30 patients with a newly diagnosed achalasia cardia in that 5-year period, with an equal incidence among men and women. The mean age of presentation was 44.63 ± 18.21 years. Malays formed the largest group. The mean weight and body mass index were 46.8 ± 10.4 kg and 18.0 ± 4.4 kg/m2 respectively. There was a wide range of duration of symptoms at presentation with a mean of 30.11 ± 35.29 months. Almost all patients presented with dysphagia (96.7%) while 70% also noted loss of weight. All patients underwent oesophagogastroduodenoscopy (OGDS) and 26 patients (86.7%) had barium swallow as part of diagnostic workup. A total of 18 patients underwent a laparoscopic Heller myotomy with or without Dor Fundoplication and/or cruroplasty while two patients (6.7%) underwent pneumatic dilatation as first treatment. Iatrogenic mucosal perforations were detected in 8 patients who underwent myotomy and fundoplication and were repaired intraoperatively. Of the patients who underwent myotomy and fundoplication, the mean weight increase was 15.6kg, increasing from 43.0 ± 8.4 kg to 58.6 ± 13.7 kg. All the patients who underwent treatment were satisfied with their treatment outcomes.
CONCLUSION: Most patients with achalasia cardia deemed suitable for surgery and counselled accordingly accept surgery resulting in high levels of satisfaction and weight gain in almost all these patients. A small minority who opt for pneumatic dilatation may also achieve satisfactory outcomes comparable to surgery in the short term. Although rare, clinicians should be able to recognise this disease early as early intervention often leads to satisfactory longterm outcomes.
METHODS: All cell populations were stained with Hoechst 33342 and analysed using dual wavelength flow cytometry to identify SP cells. This SP assay was used to assess the impact of TGF-β1 treatment and withdrawal of treatment on SP percentages. Semi-quantitative and quantitative PCR were used for molecular analysis of cells pre and post TGF-β1 treatment.
RESULTS: All cell lines expressed mRNA for both TGFB1 and its receptors, as well as showing variable expression of CDH1 and CDH2, with expressing of CDH1 being highest and CDH2 being lowest in the normal cell line. Exposure to exogenous TGF-β1 resulted in a reduction in mRNA expression of ABCG2 compared to controls which was significant between control and treated cancer cell lines. SP cells were isolated from primary human thyroid tissues, with numbers being significantly higher in papillary thyroid cancers. Exposure to TGF-β1 decreased the SP percentage in both thyroid cancer cell lines and completely abrogated these cells in the primary papillary thyroid cancer cultures. On withdrawal of TGF-β1 the SP phenotype was restored in the cancer cell lines and SP percentages increased to above that of untreated cells.
CONCLUSIONS: TGF-β1 exposure transiently regulates thyroid cancer SP cells, leading to a reduction in SP percentages, while withdrawal of TGF-β1 results in restoration of the SP phenotype.