Research on wound healing drugs is a developing area in modern biomedical sciences. Scientists who are trying to develop newer drugs from natural resources are looking toward the Ayurveda, the Indian traditional system of medicine. Several drugs of plant, mineral, and animal origin are described in the Ayurveda for their wound healing properties under the term Vranaropaka. Most of these drugs are derived from plant origin. Some of these plants have been screened scientifically for the evaluation of their wound healing activity in different pharmacological models and patients, but the potential of most remains unexplored. In a few cases, active chemical constituents were identified. Some Ayurvedic medicinal plants, namely, Ficus bengalensis, Cynodon dactylon, Symplocos racemosa, Rubia cordifolia, Pterocarpus santalinus, Ficus racemosa, Glycyrrhiza glabra, Berberis aristata, Curcuma longa, Centella asiatica, Euphorbia nerifolia, and Aloe vera, were found to be effective in experimental models. This paper presents a limited review of plants used in Ayurvedic medicine.

Plant Medicines of Indian Origin for Wound Healing Activity: A Review

Privileged scaffolds as MAO inhibitors: Retrospect and prospects.

Kaposi sarcoma–associated herpesvirus (KSHV) is linked with all clinical forms of Kaposi sarcoma and several lymphoproliferative disorders. Like other herpesviruses, KSHV becomes latent in the infected cells, expressing only a few genes that are essential for the establishment and maintenance of its latency and for the survival of the infected cells. Inhibiting the expression of these latent genes should lead to eradication of herpesvirus infection. All currently available drugs are ineffective against latent infection. Here we show, for the first time to our knowledge, that latent infection with KSHV in B lymphocytes can be terminated by glycyrrhizic acid (GA), a triterpenoid compound earlier shown to inhibit the lytic replication of other herpesviruses. We demonstrate that GA disrupts latent KSHV infection by downregulating the expression of latency-associated nuclear antigen (LANA) and upregulating the expression of viral cyclin and selectively induces cell death of KSHV-infected cells. We show that reduced levels of LANA lead to p53 reactivation, an increase in ROS, and mitochondrial dysfunction, which result in G1 cell cycle arrest, DNA fragmentation, and oxidative stress–mediated apoptosis. Latent genes are involved in KSHV-induced oncogenesis, and strategies to interfere with their expression might prove useful for eradicating latent KSHV infection and have future therapeutic implications.

/pdf/glycyrrhizic-acid-alters-kaposi-sarcoma-associated-c2e81d6vve.pdf

Glycyrrhizic acid alters Kaposi sarcoma–associated herpesvirus latency, triggering p53-mediated apoptosis in transformed B lymphocytes

In the last 2-3 decades, the broad research in the application of benzimidazole derivatives made it important for mankind. Many scientists have worked on benzimidazole derivatives and they found that this compound has a diverse role in the field of medicinal chemistry. Few benzimidazole derivatives are currently in the market as a drug candidate against various diseases. Moreover, the benzimidazole derivatives exhibit pharmacological activities such as anti-tuberculosis, anti-malarial, antihistamine, antimicrobial, antiviral, antidiabetic, anticancer, anti-fungal, anti-inflammatory, analgesic, anti-HIV, etc. In this review, we have summarized various derivatives of benzimidazole which have been prepared by many researchers to understand the chemistry as well as diverse pharmacological activities. These findings may lead the scientists who are working in the field of medicinal chemistry to the development of benzimidazole based drug candidates in the future.

Benzimidazole: A Milestone in the Field of Medicinal Chemistry.

Several pentacyclic triterpenoid metabolites of plant origin are inhibitors of hydrolysis of both synthetic peptide substrates and elastin by human leucocyte elastase (HLE). Ursolic acid, the most potent of these compounds, has an inhibition constant of 4-6 microM for hydrolysis of peptide substrates in phosphate-buffered saline. With tripeptide and tetrapeptide substrates, the inhibition is purely competitive, whereas with a shorter dipeptide substrate the inhibition is non-competitive, suggesting that ursolic acid interacts with subsite S3 of the extended substrate-binding domain in HLE, but not with subsites S1 and S2. The carboxy group at position 28 in the pentacyclic-ring system of the triterpenes contributes to binding to HLE, since replacement of this group with a hydroxy group, as in uvaol, the alcohol analogue of ursolic acid, reduces the potency of inhibition. The inhibitory potency of ursolic acid is also reduced by addition of 1 M-NaCl, further supporting a postulated electrostatic interaction between the negative charge on the triterpene and a positively charged residue on the enzyme, which we assign to the side chain of Arg-217, located in the vicinity of subsites S4 and S5 in HLE. These observations are consistent with a binding site for ursolic acid which extends from S3 towards S4 and S5 on the enzyme. Other triterpenes, including oleanolic acid, erythrodiol, hederagenin and 18 beta-glycyrrhetic acid, can also interact with this binding site. On the basis of these results we conclude that the extended substrate-binding domain of HLE can accommodate a variety of hydrophobic ligands, including not only such molecules as fatty acids [Ashe & Zimmerman (1977) Biochem. Biophys. Res. Commun. 75, 194-199; Cook & Ternai (1988) Biol. Chem. Hoppe-Seyler 369, 629-637], but also polycyclic molecules such as the pentacyclic triterpenoids.

Inhibition of human leucocyte elastase by ursolic acid. Evidence for a binding site for pentacyclic triterpenes.

Biochemical study of anti-inflammatory and anti-arthritic properties of glycyrrhetic acid

CNS depressant activity of pyrimidylthiazolidones and their selective inhibition of NAD-dependent pyruvate oxidation.

Substituted 1,5-diaryl-3(4-chlorophenyl)-delta 2-pyrazolines were synthesized and evaluated for anticonvulsant activity. Most pyrazolines (100 mg/kg) provided 20-80% protection against pentylenetetrazol-induced convulsions in mice. All compounds inhibited rat brain mitochondrial monoamine oxidase (MAO) and succinic dehydrogenase (SDH) and exhibited low toxicity as reflected by approximate LD50 values (500 to greater than 1000 mg/kg) in mice.

Inhibition of rat brain monoamine oxidase and succinic dehydrogenase by anticonvulsant pyrazolines.

Independent cholinergic and adrenergic mechanisms in the guinea-pig isolated nerve-vas deferens preparation.

Anti-inflammatory and anticonvulsant properties of some natural plant triterpenoids.

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