Materials and Methods: The experiment was divided into short-term treatment (45 days) and long-term treatment (90 days), with each group divided into nine sub-groups consisting of six animals each. Sub-groups 1 and 2 served as normal, and N-acetylcysteine (NAC) controls, respectively. Sub-groups 3-9 received sodium arsenite in drinking water (50 mg/L). In addition, sub-group 4 received NAC (210 mg/kg b.wt) orally once daily, sub-groups 5-7 received aqueous seed extract of M. pruriens (350 mg/kg b.wt, 530 mg/kg b.wt, and 700 mg/kg b.wt) orally once daily and sub-groups 8 and 9 received a combination of NAC and aqueous seed extract of M. pruriens (350 mg/kg b.wt and 530 mg/kg b.wt) orally once daily. Following the treatment, the blood was drawn retro-orbitally to assess the liver (serum alanine transaminase [ALT], serum aspartate transaminase, and serum alkaline phosphatase) and kidney (serum urea and serum creatinine) functions. Learning and memory were assessed by passive avoidance test. Animals were sacrificed by an overdose of ketamine, and their Nissl stained hippocampal sections were analyzed for alterations in neural cell numbers in CA1 and CA3 regions.
Results: In the short-term treatment, groups administered with M. pruriens 530 mg/kg b.wt alone and combination of NAC + M. pruriens 350 mg/kg b.wt exhibited a significant improvement in memory retention, less severe neurodegeneration, and decrease in serum ALT levels. In long-term treatment, groups administered with M. pruriens 700 mg/kg b.wt alone and combination of NAC+M. pruriens 350 mg/kg b.wt, respectively, showed better memory retention, decreased neural deficits, and reduced levels of kidney and liver enzymes.
Conclusion: The seed extract of M. pruriens showed significant enhancement in memory and learning. The number of surviving neurons in the CA1 and CA3 regions also increased on treatment with M. pruriens. Serum ALT, serum urea, and serum creatinine levels showed significant improvement on long-term treatment with M. pruriens.
METHODS: This was a retrospective cohort study involving two hepatobiliary centres from January 1, 2012, to June 30, 2018. Medical records were analysed for sociodemographic, clinical characteristics, laboratory testing, and HCC treatment information. Survival outcomes were examined using the Kaplan-Meier and log-rank test. Prognostic factors were determined using multivariate Cox regression.
RESULTS: A total of 212 patients were included in the study. The median survival time was 22 months. The 1-, 3-, and 5-year survival rates were 64.2%, 34.2%, and 18.0%, respectively. Palliative treatment (adjusted hazard ratio [AHR] = 2.82, 95% confidence interval [CI] 1.75-4.52), tumour size ≥ 5 cm (AHR = 2.02, 95%CI: 1.45-2.82), traditional medication (AHR = 1.94, 95%CI: 1.27-2.98), raised alkaline phosphatase (AHR = 1.74, 95%CI: 1.25-2.42), and metformin (AHR = 1.44, 95%CI: 1.03-2.00) were significantly associated with poor prognosis for HCC survival. Antiviral hepatitis treatment (AHR = 0.54, 95% CI: 0.34-0.87), nonalcoholic fatty liver disease (NAFLD) (AHR = 0.50, 95% CI: 0.30-0.84), and family history of malignancies (AHR = 0.50, 95%CI: 0.26-0.96) were identified as good prognostic factors for HCC survival.
DISCUSSION: Traditional medication, metformin treatment, advanced stage and raised alkaline phosphatase were the poor prognostic factors, while antiviral hepatitis treatment, NAFLD, and family history of malignancies were the good prognostic factors for our HCC cases comorbid with T2D.