Human liver cancer has emerged as a serious health concern in the world, associated with poorly available therapies. The Berberis genus contains vital medicinal plants with miraculous healing properties and a wide range of bioactivities. In this study, different crude extracts of B. lycium Royle were prepared and screened against Human Hepatocarcinoma (HepG2) cell lines. The water/ethanolic extract of B. lycium Royle (BLE) exhibited significant antiproliferative activity against the HepG2 cancer cell line with an IC₅₀ value of 47 μg/mL. The extract decreased the clonogenic potential of HepG2 cells in a dose‐dependent manner. It induced apoptotic cell death in HepG2 cells that were confirmed by cytometric analysis and microscopic examination of cellular morphology through DAPI‐stained cells. Biochemical evidence of apoptosis came from elevating the intracellular ROS level that was accompanied by the loss of mitochondrial membrane potential. The mechanism of apoptosis was further confirmed by gene expression analysis using RT‐qPCR that revealed the decline in Bcl‐2 independent of p53 mRNA and a rise in CDK1 while downregulating CDK5, CDK9, and CDK10 mRNA levels at 48 h of BLE treatment. The most active fraction was subjected to HPLC which indicated the presence of berberine (48 μg/mL) and benzoic acid (15.8 μg/mL) as major compounds in BLE and a trace amount of luteolin, rutin, and gallic acid. Our study highlighted the importance of the most active BLE extract as an excellent source of nutraceuticals against Human Hepatocarcinoma that can serve as an herbal natural cure against liver cancer.

Thermal decomposition characteristics and kinetics of high-density polyethylene (HDPE), corn stover (CS), and their blended mixture (1:1 w/w ratio) during non-catalytic and catalytic co-pyrolysis were studied via thermogravimetric analysis (TGA). The results indicated synergetic interactions between the biomass and the plastics during co-pyrolysis as measured by weight loss (ΔW); this effect was attributed to radical interactions during co-pyrolysis. The pyrolysis catalysts with higher nickel loadings (5%, 10%, and 15%) appreciably diminished the solid residue. Kinetic studies indicated that the pyrolysis was a first-order reaction based on the fitted thermogravimetric data. The activation energy (E) and pre-exponential factor (A) ranged between 26.13 kJ/mol to 392.67 kJ/mol and between 156.24 min-1 to 9.19 x 1023 min-1, respectively. There was a kinetic compensation effect (KCE) observed among the two kinetic parameters. The activation energy (E) decreased for each pyrolysis stage with the presence of a catalyst. The results indicated that catalytic co-pyrolysis could provide great potential for reducing the pyrolysis energy input.

Diethylamine nitrosamine (DEN), as an initiator of liver tumor, and carbon tetrachloride (CCl4), as a tumor promoter, have been used to study the molecular events of liver cancer in animal models. Recently, our in vitro study reported BLE (Berberis lycium Royle ethanol extract) as the most effective agent against liver cancer, thus we continued our study in vivo to assess the hepatoprotective effect of BLE and its most active alkaloid, berberine, in albino mice (70 male). Moreover, we investigated the biochemical/immunohistochemical effects of a single alkaloid versus the effect of Berberis extract in mice liver. Hepatic cancer was induced in mice by a single intraperitoneal injection with DEN (100 mg/kg b.wt), followed by biweekly injections of CCl₄ (0.5 mL/kg) for 30 days. The development of liver cancer was assessed after 60 days of DEN injection by measuring the elevated level of the serum tumor marker alpha-fetoprotein (AFP) and liver function test (ALT, AST, ALP, and BUN) markers. After the confirmation of liver cancer development, the BLE extract and berberine were fed to mice for 90 days and the serum biomarkers for liver injury (LFTs and AFP) were measured again. Overall, berberine (120 mg/kg b.wt) proved to be a stronger agent in reducing the symptoms of HCC in mice, as compared with BLE. Histopathological analysis agreed well with the biochemical observations. Immunohistochemistry analysis suggested significant suppression of the quantitative expression of the key oncogene cyclin D1 at low (60 mg/kg) and high (120 mg/kg) doses of berberine. These findings implicate the amelioration of hepatocarcinoma by berberine more prominently in mice, by suppression of cyclin-dependent kinase activator (CD1) expression, reducing LFTs, as well as AFP, in the serum. Thus, our findings are novel, as berberine may help in controlling the perturbation in CD1 associated with aggressive forms of HCC. However, future studies should be directed at finding out whether berberine has any effect on inhibitors (p27 and CDKI) of cyclin-dependent kinase too.