Hepatoprotective effects of walnut oil and Caralluma tuberculata against paracetamol in experimentally induced liver toxicity in mice.

Walnut Oil and Caralluma are edible and form part of the traditional medicine system in many countries. These are frequently used in traditional medicine as remedies to relieve a wide range of illnesses and health problems. Walnut Oil and Caralluma species have demonstrated anti-inflammatory, anti-nociceptive, antidiabetics, hepatoprotective, gastric mucosa protecting, antimalarial, antioxidant, anti-trypanosomal, appetite suppressant and cytotoxic activities. The current study was planned to study the impacts of 21 days' oral administration of walnut oil and methanolic extract of Caralluma tuberculata on the levels of some liver-associated parameters and hematological parameters in paracetamol intoxicated mice. It was observed that paracetamol intoxication resulted in a considerable rise in serum ALT, cholesterol, triglycerides, Creatinine, and urea levels while a decrease in HDL level in comparison to mice normal control group (P<0.05). Serum ALT, cholesterol, triglycerides, creatinine, and urea levels of mice that were administered with walnut oil and methanolic extract of C. tuberculata at the doses of (1 ml/kg, 2 ml/kg and 3 ml/kg body weight) were significantly lower when compared to toxic control mice group (P<0.05), While HDL level was significantly increased. The significant reduction had also been observed in the levels of serum parameters of mice group, which received standard hepato-protective drug i.e., vitamin C, at the dose of 8 mg/kg body weight (P<0.05). Based on these results, it was evident that liver toxicity caused by the paracetamol administration has recovered toward the normal range by the walnut oil and C. tuberculata extract. Therefore, the present study revealed that (walnut oil and C. tuberculata) exhibit hepatoprotective activities in paracetamol intoxicated mice.

Immunoinformatics Approach to Design Multi-Epitope-Based Vaccine against Machupo Virus Taking Viral Nucleocapsid as a Potential Candidate.

The family members of Arenaviridae include members of the genus Machupo virus, which have bi-segmented negative sense RNA inside the envelope and can be transferred to humans through rodent carriers. Machupo virus, a member of the mammarenavirus genus, causes Bolivian hemorrhage fever, its viral nucleocapsid protein being a significant virulence factor. Currently, no treatment is available for Bolivian hemorrhage fever and work to develop a protective as well as post-diagnosis treatment is underway. Adding to these efforts, this study employed a reverse-vaccinology approach to design a vaccine with B and T-cell epitopes of the viral nucleocapsid protein of the Machupo virus. Five B-cell specific, eight MHC-I restricted, and 14 MHC-II restricted epitopes were finalized for the construct based on an antigenicity score of >0.5 and non-allergenicity as a key characteristic. The poly-histidine tag was used to construct an immunogenic and stable vaccine construct and 50S ribosomal 46 protein L7/L12 adjuvant with linkers (EAAAK, GPGPG, and AYY). It covers 99.99% of the world's population, making it highly efficient. The physicochemical properties like the aliphatic index (118.31) and the GRAVY index (0.302) showed that the vaccine is easily soluble. The overall Ramachandran score of the construct was 90.7%, and the instability index was 35.13, endorsing a stable structure. The immune simulations demonstrated a long-lasting antibody response even after the excretion of the antigen from the body in the first 5 days of injection. The IgM + IgG titers were predicted to rise to 6000 10 days post-injection and were illustrated to be stable (around 3000) after a month, elucidating that the vaccine would be effective and provide enduring protection. Lastly, the molecular interaction between the construct and the IKBKE receptor was significant and a higher eigenfactor value in MD simulations confirmed the stable molecular interaction between the receptor and the vaccine, validating our construct.